Theodore Alan Slotkin

Journal Article Ann Biomed Eng · August 4, 2024 PURPOSE: This study aims to explore how cyclic loading influences creep response in the lumbar spine under combined flexion-compression loading. METHODS: Ten porcine functional spinal units (FSUs) were mechanically tested in cyclic or static combined flexi ... Full text Link to item Cite

Mohamed Bahie Abou-Donia: Pioneer in organophosphorus-induced neurotoxicity.

Journal Article Neurotoxicology · January 2024 Full text Link to item Cite

Analysing Biomechanical Response Curves and How Statistics Expose Physiology

Conference Conference proceedings International Research Council on the Biomechanics of Injury, IRCOBI · January 1, 2024 Cite

Developmental exposure to the flame retardant, triphenyl phosphate, causes long-lasting neurobehavioral and neurochemical dysfunction.

Journal Article Birth Defects Res · February 1, 2023 BACKGROUND: Human exposures to organophosphate flame retardants result from their use as additives in numerous consumer products. These agents are replacements for brominated flame retardants but have not yet faced similar scrutiny for developmental neurot ... Full text Open Access Link to item Cite

Temporally non-regular patterns of deep brain stimulation (DBS) enhance assessment of evoked potentials while maintaining motor symptom management in Parkinson's disease (PD).

Journal Article Brain Stimul · 2023 BACKGROUND: Traditional deep brain stimulation (DBS) at fixed regular frequencies (>100 Hz) is effective in treating motor symptoms of Parkinson's disease (PD). Temporally non-regular patterns of DBS are a new parameter space that may help increase efficac ... Full text Link to item Cite

Persistent neurobehavioral and neurochemical anomalies in middle-aged rats after maternal diazinon exposure.

Journal Article Toxicology · April 30, 2022 Diazinon is an organophosphate pesticide that has a history of wide use. Developmental exposures to organophosphates lead to neurobehavioral changes that emerge early in life and can persist into adulthood. However, preclinical studies have generally evalu ... Full text Open Access Link to item Cite

Paternal Cannabis Exposure Prior to Mating, but Not Δ9-Tetrahydrocannabinol, Elicits Deficits in Dopaminergic Synaptic Activity in the Offspring.

Journal Article Toxicol Sci · November 24, 2021 The legalization and increasing availability of cannabis products raises concerns about the impact on offspring of users, and little has appeared on the potential contribution of paternal use. We administered cannabis extract to male rats prior to mating, ... Full text Open Access Link to item Cite

Analysis of polycyclic aromatic hydrocarbon intake in the US adult population from NHANES 2005-2014 identifies vulnerable subpopulations, suggests interaction between tobacco smoke exposure and sociodemographic factors.

Journal Article Environ Res · October 2021 Polycyclic aromatic hydrocarbons (PAHs) are a toxic and ubiquitous class of environmental chemicals, products of fuel combustion from human and natural sources. The objective of this study was to identify vulnerable populations for high PAH exposure and va ... Full text Link to item Cite

Neurobehavioral anomalies in zebrafish after sequential exposures to DDT and chlorpyrifos in adulthood: Do multiple exposures interact?

Journal Article Neurotoxicol Teratol · 2021 A sequence of different classes of synthetic insecticides have been used over the past 70 years. Over this period, the widely-used organochlorines were eventually replaced by organophosphates, with dichlorodiphenyltrichloroethane (DDT) and chlorpyrifos (CP ... Full text Open Access Link to item Cite

Abstract D093: Who carries the excess cancer risk burden: Implications of disparities in polycyclic aromatic hydrocarbon exposure

Conference Cancer Epidemiology, Biomarkers & Prevention · June 1, 2020 AbstractPolycyclic aromatic hydrocarbons (PAHs) are a toxic and ubiquitous class of environmental chemicals sourced from industrial practices, tobacco smoke, grilled and smoked meats, car exhaust, and other ... Full text Cite

Paternal Δ9-Tetrahydrocannabinol Exposure Prior to Mating Elicits Deficits in Cholinergic Synaptic Function in the Offspring.

Journal Article Toxicol Sci · April 1, 2020 Little attention has been paid to the potential impact of paternal marijuana use on offspring brain development. We administered Δ9-tetrahydrocannabinol (THC, 0, 2, or 4 mg/kg/day) to male rats for 28 days. Two days after the last THC treatment, the males ... Full text Open Access Link to item Cite

Adult exposure to insecticides causes persistent behavioral and neurochemical alterations in zebrafish.

Journal Article Neurotoxicol Teratol · 2020 Farmers are often chronically exposed to insecticides, which may present health risks including increased risk of neurobehavioral impairment during adulthood and across aging. Experimental animal studies complement epidemiological studies to help determine ... Full text Open Access Link to item Cite

Perinatal diazinon exposure compromises the development of acetylcholine and serotonin systems.

Journal Article Toxicology · August 1, 2019 Organophosphate pesticides are developmental neurotoxicants. We gave diazinon via osmotic minipumps implanted into dams prior to conception, with exposure continued into the second postnatal week, at doses (0.5 or 1 mg/kg/day) that did not produce detectab ... Full text Open Access Link to item Cite

Corrigendum to "The Developmental Neurotoxicity of Tobacco Smoke Can Be Mimicked by a Combination of Nicotine and Benzo[a]pyrene: Effects on Cholinergic and Serotonergic Systems".

Journal Article Toxicol Sci · March 1, 2019 Full text Open Access Link to item Cite

The Developmental Neurotoxicity of Tobacco Smoke Can Be Mimicked by a Combination of Nicotine and Benzo[a]Pyrene: Effects on Cholinergic and Serotonergic Systems.

Journal Article Toxicol Sci · January 1, 2019 Tobacco smoke contains polycyclic aromatic hydrocarbons (PAHs) in addition to nicotine. We compared the developmental neurotoxicity of nicotine to that of the PAH archetype, benzo[a]pyrene (BaP), and also evaluated the effects of combined exposure to asses ... Full text Open Access Link to item Cite

Does growth impairment underlie the adverse effects of dexamethasone on development of noradrenergic systems?

Journal Article Toxicology · September 1, 2018 Glucocorticoids are given in preterm labor to prevent respiratory distress but these agents evoke neurobehavioral deficits in association with reduced brain region volumes. To determine whether the neurodevelopmental effects are distinct from growth impair ... Full text Link to item Cite

Critical developmental periods for effects of low-level tobacco smoke exposure on behavioral performance.

Journal Article Neurotoxicology · September 2018 Tobacco exposure during development leads to neurobehavioral dysfunction in children, even when exposure is limited to secondhand smoke. We have previously shown in rats that developmental exposure to tobacco smoke extract (TSE), at levels mimicking second ... Full text Open Access Link to item Cite

Developmental neurotoxicity resulting from pharmacotherapy of preterm labor, modeled in vitro: Terbutaline and dexamethasone, separately and together.

Journal Article Toxicology · May 1, 2018 Terbutaline and dexamethasone are used in the management of preterm labor, often for durations of treatment exceeding those recommended, and both have been implicated in increased risk of neurodevelopmental disorders. We used a variety of cell models to es ... Full text Link to item Cite

Brominated and organophosphate flame retardants target different neurodevelopmental stages, characterized with embryonic neural stem cells and neuronotypic PC12 cells.

Journal Article Toxicology · September 1, 2017 In addition to their activity as endocrine disruptors, brominated and organophosphate flame retardants are suspected to be developmental neurotoxicants, although identifying their specific mechanisms for that activity has been elusive. In the current study ... Full text Link to item Cite

Diazinon and parathion diverge in their effects on development of noradrenergic systems.

Journal Article Brain Res Bull · April 2017 Organophosphate pesticides elicit developmental neurotoxicity through mechanisms over and above their shared property as cholinesterase inhibitors. We compared the consequences of neonatal exposure (postnatal days PN1-4) to diazinon or parathion on develop ... Full text Link to item Cite

Cyclic Mechanism Affects Lumbar Spine Creep Response.

Mohamed Bahie Abou-Donia: Pioneer in organophosphorus-induced neurotoxicity.

Journal Article Neurotoxicology · January 2024 Full text Link to item Cite

Analysing Biomechanical Response Curves and How Statistics Expose Physiology

Conference Conference proceedings International Research Council on the Biomechanics of Injury, IRCOBI · January 1, 2024 Cite

Developmental exposure to the flame retardant, triphenyl phosphate, causes long-lasting neurobehavioral and neurochemical dysfunction.

Temporally non-regular patterns of deep brain stimulation (DBS) enhance assessment of evoked potentials while maintaining motor symptom management in Parkinson's disease (PD).

Persistent neurobehavioral and neurochemical anomalies in middle-aged rats after maternal diazinon exposure.

Paternal Cannabis Exposure Prior to Mating, but Not Δ9-Tetrahydrocannabinol, Elicits Deficits in Dopaminergic Synaptic Activity in the Offspring.

Analysis of polycyclic aromatic hydrocarbon intake in the US adult population from NHANES 2005-2014 identifies vulnerable subpopulations, suggests interaction between tobacco smoke exposure and sociodemographic factors.

Neurobehavioral anomalies in zebrafish after sequential exposures to DDT and chlorpyrifos in adulthood: Do multiple exposures interact?

Abstract D093: Who carries the excess cancer risk burden: Implications of disparities in polycyclic aromatic hydrocarbon exposure

Paternal Δ9-Tetrahydrocannabinol Exposure Prior to Mating Elicits Deficits in Cholinergic Synaptic Function in the Offspring.

Adult exposure to insecticides causes persistent behavioral and neurochemical alterations in zebrafish.

Perinatal diazinon exposure compromises the development of acetylcholine and serotonin systems.

Corrigendum to "The Developmental Neurotoxicity of Tobacco Smoke Can Be Mimicked by a Combination of Nicotine and Benzo[a]pyrene: Effects on Cholinergic and Serotonergic Systems".

Journal Article Toxicol Sci · March 1, 2019 Full text Open Access Link to item Cite

The Developmental Neurotoxicity of Tobacco Smoke Can Be Mimicked by a Combination of Nicotine and Benzo[a]Pyrene: Effects on Cholinergic and Serotonergic Systems.

Does growth impairment underlie the adverse effects of dexamethasone on development of noradrenergic systems?

Critical developmental periods for effects of low-level tobacco smoke exposure on behavioral performance.

Developmental neurotoxicity resulting from pharmacotherapy of preterm labor, modeled in vitro: Terbutaline and dexamethasone, separately and together.

Brominated and organophosphate flame retardants target different neurodevelopmental stages, characterized with embryonic neural stem cells and neuronotypic PC12 cells.

Diazinon and parathion diverge in their effects on development of noradrenergic systems.

In vitro models reveal differences in the developmental neurotoxicity of an environmental polycylic aromatic hydrocarbon mixture compared to benzo[a]pyrene: Neuronotypic PC12 Cells and embryonic neural stem cells.

Journal Article Toxicology · February 15, 2017 In addition to their carcinogenic activity, polycyclic aromatic hydrocarbons (PAHs) are suspected to be developmental neurotoxicants. We evaluated the effects of PAHs with two in vitro models that assess distinct "decision nodes" in neurodifferentiation: n ... Full text Link to item Cite

Is There a Critical Period for the Developmental Neurotoxicity of Low-Level Tobacco Smoke Exposure?

Journal Article Toxicol Sci · January 2017 Secondhand tobacco smoke exposure in pregnancy increases the risk of neurodevelopmental disorders. We evaluated in rats whether there is a critical period during which tobacco smoke extract (TSE) affects the development of acetylcholine and serotonin syste ... Full text Open Access Link to item Cite

Developmental toxicity of nicotine: A transdisciplinary synthesis and implications for emerging tobacco products.

Journal Article Neurosci Biobehav Rev · January 2017 While the health risks associated with adult cigarette smoking have been well described, effects of nicotine exposure during periods of developmental vulnerability are often overlooked. Using MEDLINE and PubMed literature searches, books, reports and exper ... Full text Link to item Cite

Diverse neurotoxicants target the differentiation of embryonic neural stem cells into neuronal and glial phenotypes.

Journal Article Toxicology · November 30, 2016 The large number of compounds that needs to be tested for developmental neurotoxicity drives the need to establish in vitro models to evaluate specific neurotoxic endpoints. We used neural stem cells derived from rat neuroepithelium on embryonic day 14 to ... Full text Link to item Cite

Cognitive and Behavioral Impairments Evoked by Low-Level Exposure to Tobacco Smoke Components: Comparison with Nicotine Alone.

Journal Article Toxicol Sci · June 2016 Active maternal smoking has adverse effects on neurobehavioral development of the offspring, with nicotine (Nic) providing much of the underlying causative mechanism. To determine whether the lower exposures caused by second-hand smoke are deleterious, we ... Full text Open Access Link to item Cite

Adolescents and adults differ in the immediate and long-term impact of nicotine administration and withdrawal on cardiac norepinephrine.

Journal Article Brain Res Bull · April 2016 Cardiovascular responses to smoking cessation may differ in adolescents compared to adults. We administered nicotine by osmotic minipump infusion for 17 days to adolescent and adult rats (30 and 90 days of age, respectively) and examined cardiac norepineph ... Full text Link to item Cite

Prenatal drug exposures sensitize noradrenergic circuits to subsequent disruption by chlorpyrifos.

Journal Article Toxicology · December 2, 2015 We examined whether nicotine or dexamethasone, common prenatal drug exposures, sensitize the developing brain to chlorpyrifos. We gave nicotine to pregnant rats throughout gestation at a dose (3mg/kg/day) producing plasma levels typical of smokers; offspri ... Full text Link to item Cite

Developmental Neurotoxicity of Tobacco Smoke Directed Toward Cholinergic and Serotonergic Systems: More Than Just Nicotine.

Journal Article Toxicol Sci · September 2015 Tobacco smoke contains thousands of compounds in addition to nicotine, a known neuroteratogen. We evaluated the developmental neurotoxicity of tobacco smoke extract (TSE) administered to pregnant rats starting preconception and continued through the second ... Full text Link to item Cite

Amelioration strategies fail to prevent tobacco smoke effects on neurodifferentiation: Nicotinic receptor blockade, antioxidants, methyl donors.

Journal Article Toxicology · July 3, 2015 Tobacco smoke exposure is associated with neurodevelopmental disorders. We used neuronotypic PC12 cells to evaluate the mechanisms by which tobacco smoke extract (TSE) affects neurodifferentiation. In undifferentiated cells, TSE impaired DNA synthesis and ... Full text Link to item Cite

Prenatal nicotine changes the response to postnatal chlorpyrifos: Interactions targeting serotonergic synaptic function and cognition.

Journal Article Brain Res Bull · February 2015 Nicotine and chlorpyrifos are developmental neurotoxicants that target serotonin systems. We examined whether prenatal nicotine exposure alters the subsequent response to chlorpyrifos given postnatally. Pregnant rats received nicotine throughout gestation ... Full text Link to item Cite

Prenatal nicotine alters the developmental neurotoxicity of postnatal chlorpyrifos directed toward cholinergic systems: better, worse, or just "different?".

Journal Article Brain Res Bull · January 2015 This study examines whether prenatal nicotine exposure sensitizes the developing brain to subsequent developmental neurotoxicity evoked by chlorpyrifos, a commonly-used insecticide. We gave nicotine to pregnant rats throughout gestation at a dose (3mg/kg/d ... Full text Link to item Cite

Sex-selective interaction of prenatal nicotine with neonatal chlorpyrifos on novel object recognition in rats

Conference Neurotoxicology and Teratology · May 2014 Full text Cite

Nicotine administration in adolescence reprograms the subsequent response to nicotine treatment and withdrawal in adulthood: sex-selective effects on cerebrocortical serotonergic function.

Journal Article Brain Res Bull · March 2014 Nicotine exposure in adolescence produces lasting changes in subsequent behavioral responses to addictive agents. We gave nicotine to adolescent rats (postnatal days PN30-47), simulating plasma levels in smokers, and then examined the subsequent effects of ... Full text Link to item Cite

Prenatal dexamethasone, as used in preterm labor, worsens the impact of postnatal chlorpyrifos exposure on serotonergic pathways.

Journal Article Brain Res Bull · January 2014 This study explores how glucocorticoids sensitize the developing brain to the organophosphate pesticide, chlorpyrifos. Pregnant rats received a standard therapeutic dose (0.2mg/kg) of dexamethasone on gestational days 17-19; pups were given subtoxic doses ... Full text Link to item Cite

Effects of tobacco smoke on PC12 cell neurodifferentiation are distinct from those of nicotine or benzo[a]pyrene.

Journal Article Neurotoxicol Teratol · 2014 Although nicotine accounts for a great deal of the neurodevelopmental damage associated with maternal smoking or second-hand exposure, tobacco smoke contains thousands of potentially neurotoxic compounds. We used PC12 cells, a standard in vitro model of ne ... Full text Link to item Cite

Prenatal dexamethasone augments the neurobehavioral teratology of chlorpyrifos: significance for maternal stress and preterm labor.

Journal Article Neurotoxicol Teratol · 2014 Glucocorticoids are the consensus treatment given in preterm labor and are also elevated by maternal stress; organophosphate exposures are virtually ubiquitous, so human developmental coexposures to these two agents are common. This study explores how pren ... Full text Link to item Cite

Does thyroid disruption contribute to the developmental neurotoxicity of chlorpyrifos?

Journal Article Environ Toxicol Pharmacol · September 2013 Although organophosphate pesticides are not usually characterized as "endocrine disruptors," recent work points to potential, long-term reductions of circulating thyroid hormones after developmental exposures to chlorpyrifos that are devoid of observable t ... Full text Link to item Cite

Maternal smoking and conduct disorder in the offspring.

Journal Article JAMA Psychiatry · September 2013 Full text Link to item Cite

Adverse benzo[a]pyrene effects on neurodifferentiation are altered by other neurotoxicant coexposures: interactions with dexamethasone, chlorpyrifos, or nicotine in PC12 cells.

Journal Article Environ Health Perspect · July 2013 BACKGROUND: Polycyclic aromatic hydrocarbons are suspected developmental neurotoxicants, but human exposures typically occur in combination with other neurotoxic contaminants. OBJECTIVE AND METHODS: We explored the effects of benzo[a]pyrene (BaP) on neurod ... Full text Link to item Cite

Prenatal dexamethasone augments the sex-selective developmental neurotoxicity of chlorpyrifos: Implications for vulnerability after pharmacotherapy for preterm labor

Journal Article NEUROTOXICOLOGY AND TERATOLOGY · May 1, 2013 Full text Link to item Cite

Branched-chain amino acids alter neurobehavioral function in rats.

Journal Article Am J Physiol Endocrinol Metab · February 15, 2013 Recently, we have described a strong association of branched-chain amino acids (BCAA) and aromatic amino acids (AAA) with obesity and insulin resistance. In the current study, we have investigated the potential impact of BCAA on behavioral functions. We de ... Full text Link to item Cite

Evaluation of the association between maternal smoking, childhood obesity, and metabolic disorders: a national toxicology program workshop review.

Journal Article Environ Health Perspect · February 2013 BACKGROUND: An emerging literature suggests that environmental chemicals may play a role in the development of childhood obesity and metabolic disorders, especially when exposure occurs early in life. OBJECTIVE: Here we assess the association between these ... Full text Open Access Link to item Cite

Terbutaline impairs the development of peripheral noradrenergic projections: potential implications for autism spectrum disorders and pharmacotherapy of preterm labor.

Journal Article Neurotoxicol Teratol · 2013 Terbutaline, a β2-adrenoceptor agonist, is used off-label for long-term management of preterm labor; such use is associated with increased risk of neurodevelopmental disorders, including autism spectrum disorders. We explored the mechanisms underlying terb ... Full text Link to item Cite

BDE99 (2,2',4,4',5-pentabromodiphenyl ether) suppresses differentiation into neurotransmitter phenotypes in PC12 cells.

Journal Article Neurotoxicol Teratol · 2013 Early-life exposures to brominated diphenyl ethers (BDEs) lead to neurobehavioral abnormalities later in life. Although these agents are thyroid disruptors, it is not clear whether this mechanism alone accounts for the adverse effects. We evaluated the imp ... Full text Link to item Cite

Prenatal dexamethasone augments the sex-selective developmental neurotoxicity of chlorpyrifos: implications for vulnerability after pharmacotherapy for preterm labor.

Journal Article Neurotoxicol Teratol · 2013 Glucocorticoids are routinely given in preterm labor and are also elevated by maternal stress; organophosphate exposures are virtually ubiquitous, so coexposures to these two agents are pervasive. We administered dexamethasone to pregnant rats on gestation ... Full text Link to item Cite

Reply to Juberg: Using the biologically based dose response to compare exposures across species

Journal Article Proceedings of the National Academy of Sciences of the United States of America · August 14, 2012 Full text Cite

Does mechanism matter? Unrelated neurotoxicants converge on cell cycle and apoptosis during neurodifferentiation.

Journal Article Neurotoxicol Teratol · July 2012 Mechanistically unrelated developmental neurotoxicants often produce neural cell loss culminating in similar functional and behavioral outcomes. We compared an organophosphate pesticide (diazinon), an organochlorine pesticide (dieldrin) and a metal (Ni(2+) ... Full text Link to item Cite

Brain anomalies in children exposed prenatally to a common organophosphate pesticide.

Journal Article Proc Natl Acad Sci U S A · May 15, 2012 Prenatal exposure to chlorpyrifos (CPF), an organophosphate insecticide, is associated with neurobehavioral deficits in humans and animal models. We investigated associations between CPF exposure and brain morphology using magnetic resonance imaging in 40 ... Full text Link to item Cite

Developmental neurotoxicity of organophosphates targets cell cycle and apoptosis, revealed by transcriptional profiles in vivo and in vitro.

Journal Article Neurotoxicol Teratol · March 2012 Developmental organophosphate exposure reduces the numbers of neural cells, contributing to neurobehavioral deficits. We administered chlorpyrifos or diazinon to newborn rats on postnatal days 1-4, in doses straddling the threshold for barely-detectable ch ... Full text Link to item Cite

Chlorpyrifos developmental neurotoxicity: interaction with glucocorticoids in PC12 cells.

Journal Article Neurotoxicol Teratol · 2012 Prenatal coexposures to glucocorticoids and organophosphate pesticides are widespread. Glucocorticoids are elevated by maternal stress and are commonly given in preterm labor; organophosphate exposures are virtually ubiquitous. We used PC12 cells undergoin ... Full text Link to item Cite

Developmental exposure to organophosphates triggers transcriptional changes in genes associated with Parkinson's disease in vitro and in vivo.

Journal Article Brain Res Bull · November 25, 2011 Epidemiologic studies support a connection between organophosphate pesticide exposures and subsequent risk of Parkinson's disease (PD). We used differentiating, neuronotypic PC12 cells to compare organophosphates (chlorpyrifos, diazinon), an organochlorine ... Full text Link to item Cite

Mimicking maternal smoking and pharmacotherapy of preterm labor: fetal nicotine exposure enhances the effect of late gestational dexamethasone treatment on noradrenergic circuits.

Journal Article Brain Res Bull · November 25, 2011 Smoking during pregnancy increases the risk of preterm delivery, which in turn necessitates the common use of glucocorticoids to prevent respiratory distress syndrome. Accordingly, there is a substantial population exposed conjointly to fetal nicotine and ... Full text Link to item Cite

Is the PentaBDE replacement, tris (1,3-dichloro-2-propyl) phosphate (TDCPP), a developmental neurotoxicant? Studies in PC12 cells.

Journal Article Toxicol Appl Pharmacol · November 1, 2011 Organophosphate flame retardants (OPFRs) are used as replacements for the commercial PentaBDE mixture that was phased out in 2004. OPFRs are ubiquitous in the environment and detected at high concentrations in residential dust, suggesting widespread human ... Full text Link to item Cite

Concerning "Absence of neurotoxicity with medicinal grade terbutaline in the rat model," by M.Y. Owens, K.L. Wallace, N. Mamoon, J. Wyatt-Ashmead and W.A. Bennett.

Journal Article Reprod Toxicol · November 2011 Full text Link to item Cite

Reversal of chlorpyrifos neurobehavioral teratogenicity in mice by allographic transplantation of adult subventricular zone-derived neural stem cells.

Journal Article J Neurosci Res · August 2011 Neurobehavioral teratogenicity can be reversed with transplantation of neural stem cells. However, the usefulness of this therapy would be greatly enhanced by employing adult stem cells. In pursuit of this this goal, we developed a model that uses subventr ... Full text Link to item Cite

Avian Models for Neurobehavioral Teratogenicity and Its Reversal by Stem Cell Transplantation

Conference Neurotoxicology and Teratology · July 2011 Full text Cite

Developmental neurotoxicity targeting hepatic and cardiac sympathetic innervation: effects of organophosphates are distinct from those of glucocorticoids.

Journal Article Brain Res Bull · May 30, 2011 Early-life exposure to organophosphate pesticides leads to subsequent hyperresponsiveness of β-adrenergic receptor-mediated cell signaling that regulates hepatic gluconeogenesis, culminating in metabolic abnormalities resembling prediabetes. In the current ... Full text Link to item Cite

Does early-life exposure to organophosphate insecticides lead to prediabetes and obesity?

Journal Article Reprod Toxicol · April 2011 Human exposures to organophosphate insecticides are ubiquitous. Although regarded as neurotoxicants, increasing evidence points toward lasting metabolic disruption from early-life organophosphate exposures. We gave neonatal rats chlorpyrifos, diazinon or p ... Full text Link to item Cite

Silver exposure in developing zebrafish produces persistent synaptic and behavioral changes.

Journal Article Neurotoxicol Teratol · 2011 Environmental silver exposures are increasing due to the use of silver nanoparticles, which exert antimicrobial actions by releasing Ag+, a suspected developmental neurotoxicant. We evaluated the long-term neurochemical and behavioral effects of embryonic ... Full text Link to item Cite

Silver nanoparticles alter zebrafish development and larval behavior: distinct roles for particle size, coating and composition.

Journal Article Neurotoxicol Teratol · 2011 Silver nanoparticles (AgNPs) act as antibacterials by releasing monovalent silver (Ag(+)) and are increasingly used in consumer products, thus elevating exposures in human and wildlife populations. In vitro models indicate that AgNPs are likely to be devel ... Full text Link to item Cite

Prenatal nicotine exposure in rhesus monkeys compromises development of brainstem and cardiac monoamine pathways involved in perinatal adaptation and sudden infant death syndrome: amelioration by vitamin C.

Journal Article Neurotoxicol Teratol · 2011 Maternal smoking during pregnancy greatly enhances perinatal morbidity/mortality and is the major risk factor for Sudden Infant Death Syndrome (SIDS). Studies in developing rodents indicate that nicotine is a neuroteratogen that targets monoamine pathways ... Full text Link to item Cite

Silver nanoparticles compromise neurodevelopment in PC12 cells: critical contributions of silver ion, particle size, coating, and composition.

Journal Article Environ Health Perspect · January 2011 BACKGROUND: Silver exposures are rising because of the increased use of silver nanoparticles (AgNPs) in consumer products. The monovalent silver ion (Ag+) impairs neurodevelopment in PC12 cells and zebrafish. OBJECTIVES AND METHODS: We compared the effects ... Full text Link to item Cite

Diverse neurotoxicants converge on gene expression for neuropeptides and their receptors in an in vitro model of neurodifferentiation: effects of chlorpyrifos, diazinon, dieldrin and divalent nickel in PC12 cells.

Journal Article Brain Res · September 24, 2010 Unrelated developmental neurotoxicants can produce similar neurobehavioral outcomes. We examined whether disparate agents affect neuromodulators that control numerous neurotransmitters and circuits, employing PC12 cells to explore the targeting of neuroact ... Full text Link to item Cite

Transcriptional profiles for glutamate transporters reveal differences between organophosphates but similarities with unrelated neurotoxicants.

Journal Article Brain Res Bull · August 30, 2010 The developmental neurotoxicity of organophosphates involves mechanisms other than their shared property as cholinesterase inhibitors, among which are excitotoxicity and oxidative stress. We used PC12 cells as a neurodevelopmental model to compare the effe ... Full text Link to item Cite

Acute spinal cord injury persistently reduces R/G RNA editing of AMPA receptors.

Journal Article J Neurochem · July 2010 Spinal cord injury (SCI) triggers a complex ischemic and inflammatory reaction, involving activation of neurotransmitter systems, in particular glutamate, culminating in cell death. We hypothesized that SCI might lead to alteration in the RNA editing of al ... Full text Link to item Cite

Organophosphate exposure during a critical developmental stage reprograms adenylyl cyclase signaling in PC12 cells.

Journal Article Brain Res · May 6, 2010 Early-life organophosphate (OP) exposures elicit neurobehavioral deficits through mechanisms other than inhibiting cholinesterase. Cell signaling cascades are postulated as critical noncholinesterase targets that mediate both the initial alterations in neu ... Full text Link to item Cite

Mimicking maternal smoking and pharmacotherapy of preterm labor: interactions of fetal nicotine and dexamethasone on serotonin and dopamine synaptic function in adolescence and adulthood.

Journal Article Brain Res Bull · April 29, 2010 Fetal coexposure to nicotine and dexamethasone is common: maternal smoking increases the incidence of preterm delivery and glucocorticoids are the consensus treatment for prematurity. We gave pregnant rats 3mg/kg/day of nicotine throughout gestation, a reg ... Full text Link to item Cite

Neonatal parathion exposure and interactions with a high-fat diet in adulthood: Adenylyl cyclase-mediated cell signaling in heart, liver and cerebellum.

Journal Article Brain Res Bull · April 5, 2010 Organophosphates are developmental neurotoxicants but recent evidence points to additional adverse effects on metabolism and cardiovascular function. One common mechanism is disrupted cell signaling mediated through cyclic AMP, targeting neurohumoral recep ... Full text Link to item Cite

Additive and synergistic effects of fetal nicotine and dexamethasone exposure on cholinergic synaptic function in adolescence and adulthood: Implications for the adverse consequences of maternal smoking and pharmacotherapy of preterm delivery.

Journal Article Brain Res Bull · April 5, 2010 Maternal smoking contributes to preterm delivery; glucocorticoids are the consensus treatment for prematurity, thus producing fetal coexposure to nicotine and dexamethasone. We administered nicotine to pregnant rats throughout gestation at a dose (3 mg/kg/ ... Full text Link to item Cite

Early postnatal parathion exposure in rats causes sex-selective cognitive impairment and neurotransmitter defects which emerge in aging.

Journal Article Behav Brain Res · April 2, 2010 Developmental exposure of rats to the organophosphate (OP) pesticides leads to altered neurobehavioral function in juvenile and young adult stages. The current study was conducted to determine whether effects of neonatal parathion exposure on cognitive per ... Full text Link to item Cite

Disparate developmental neurotoxicants converge on the cyclic AMP signaling cascade, revealed by transcriptional profiles in vitro and in vivo.

Journal Article Brain Res · February 26, 2010 Cell-signaling cascades are convergent targets for developmental neurotoxicity of otherwise unrelated agents. We compared organophosphates (chlorpyrifos, diazinon), an organochlorine (dieldrin) and a metal (Ni(2+)) for their effects on neuronotypic PC12 ce ... Full text Link to item Cite

Neonatal organophosphorus pesticide exposure alters the developmental trajectory of cell-signaling cascades controlling metabolism: differential effects of diazinon and parathion.

Journal Article Environ Health Perspect · February 2010 BACKGROUND: Organophosphorus pesticides (OPs) are developmental neurotoxicants but also produce lasting effects on metabolism. OBJECTIVES/METHODS: We administered diazinon (DZN) or parathion (PRT) to rats on postnatal days 14 at doses straddling the thresh ... Full text Link to item Cite

Neonatal exposure to parathion alters lipid metabolism in adulthood: Interactions with dietary fat intake and implications for neurodevelopmental deficits.

Journal Article Brain Res Bull · January 15, 2010 Organophosphates are developmental neurotoxicants but recent evidence also points to metabolic dysfunction. We determined whether neonatal parathion exposure in rats has long-term effects on regulation of adipokines and lipid peroxidation. We also assessed ... Full text Link to item Cite

Silver exposure in developing zebrafish (Danio rerio): persistent effects on larval behavior and survival.

Journal Article Neurotoxicol Teratol · 2010 The increased use of silver nanoparticles in consumer and medical products has led to elevated human and environmental exposures. Silver nanoparticles act as antibacterial/antifungal agents by releasing Ag(+) and recent studies show that Ag(+) impairs neur ... Full text Link to item Cite

Neonatal dexamethasone treatment leads to alterations in cell signaling cascades controlling hepatic and cardiac function in adulthood.

Journal Article Neurotoxicol Teratol · 2010 Increasing evidence indicates that early-life glucocorticoid exposure, either involving stress or the therapy of preterm labor, contributes to metabolic and cardiovascular disorders in adulthood. We investigated cellular mechanisms underlying these effects ... Full text Link to item Cite

Oxidative stress from diverse developmental neurotoxicants: antioxidants protect against lipid peroxidation without preventing cell loss.

Journal Article Neurotoxicol Teratol · 2010 Oxidative stress has been hypothesized to provide a mechanism by which apparently unrelated chemicals can nevertheless produce similar developmental neurotoxic outcomes. We used differentiating PC12 cells to compare the effects of agents from four differen ... Full text Link to item Cite

Silver impairs neurodevelopment: studies in PC12 cells.

Journal Article Environ Health Perspect · January 2010 BACKGROUND: Exposure to silver is increasing because of silver nanoparticles in consumer products. OBJECTIVES AND METHODS: Many biological effects of silver entail actions of Ag+ (monovalent silver ions), so we used neuronotypic PC12 cells to evaluate the ... Full text Link to item Cite

Unrelated developmental neurotoxicants elicit similar transcriptional profiles for effects on neurotrophic factors and their receptors in an in vitro model.

Journal Article Neurotoxicol Teratol · 2010 Diverse developmental neurotoxicants can often produce similar functional and behavioral outcomes. We examined an organophosphate pesticide (diazinon), an organochlorine pesticide (dieldrin) and a metal (Ni(2+)) for effects on the expression of neurotrophi ... Full text Link to item Cite

An avian model for the reversal of neurobehavioral teratogenicity with neural stem cells.

Journal Article Neurotoxicol Teratol · 2010 A fast and simple model which uses lower animals on the evolutionary scale is beneficial for developing procedures for the reversal of neurobehavioral teratogenicity with neural stem cells. Here, we established a procedure for the derivation of chick neura ... Full text Link to item Cite

Neurobehavioral teratogenicity of perfluorinated alkyls in an avian model.

Journal Article Neurotoxicol Teratol · 2010 Perfluorinated alkyls are widely-used agents that accumulate in ecosystems and organisms because of their slow rate of degradation. There is increasing concern that these agents may be developmental neurotoxicants and the present study was designed to deve ... Full text Link to item Cite

A mechanism-based complementary screening approach for the amelioration and reversal of neurobehavioral teratogenicity.

Journal Article Neurotoxicol Teratol · 2010 The identification of mechanisms and outcomes for neurobehavioral teratogenesis is critical to our ability to develop therapies to ameliorate or reverse the deleterious effects of exposure to developmental neurotoxicants. We established mechanistically-bas ... Full text Link to item Cite

Reversal of chlorpyrifos neurobehavioral teratogenicity in mice by nicotine administration and neural stem cell transplantation.

Journal Article Behav Brain Res · December 28, 2009 Identifying the mechanisms underlying the adverse effects of developmental neurotoxicants enables the design of therapies that can potentially reverse neurobehavioral deficits in adulthood. We administered chlorpyrifos (CPF), a model organophosphate pestic ... Full text Link to item Cite

Benzo[a]pyrene impairs neurodifferentiation in PC12 cells.

Journal Article Brain Res Bull · August 28, 2009 Animal studies indicate neurobehavioral anomalies after prenatal exposure to benzo[a]pyrene (BaP). In order to determine if BaP directly affects neurodevelopment, we compared its effects to those of the organophosphate insecticide, chlorpyrifos (CPF), in u ... Full text Link to item Cite

Consumption of a high-fat diet in adulthood ameliorates the effects of neonatal parathion exposure on acetylcholine systems in rat brain regions.

Journal Article Environ Health Perspect · June 2009 BACKGROUND: Developmental exposure to a wide variety of developmental neurotoxicants, including organophosphate pesticides, evokes late-emerging and persistent abnormalities in acetylcholine (ACh) systems. We are seeking interventions that can ameliorate o ... Full text Link to item Cite

Oxidative and excitatory mechanisms of developmental neurotoxicity: transcriptional profiles for chlorpyrifos, diazinon, dieldrin, and divalent nickel in PC12 cells.

Journal Article Environ Health Perspect · April 2009 BACKGROUND: Oxidative stress and excitotoxicity underlie the developmental neurotoxicity of numerous chemicals. OBJECTIVES: We compared the effects of organophosphates (chlorpyrifos and diazinon), an organo-chlorine (dieldrin), and a metal [divalent nickel ... Full text Link to item Cite

Protein kinase C is a target for diverse developmental neurotoxicants: transcriptional responses to chlorpyrifos, diazinon, dieldrin and divalent nickel in PC12 cells.

Journal Article Brain Res · March 31, 2009 Unrelated developmental neurotoxicants can elicit similar functional outcomes, whereas agents in the same class may differ. We compared two organophosphate insecticides (chlorpyrifos, diazinon) with an organochlorine (dieldrin) and a metal (Ni(2+)) for sim ... Full text Link to item Cite

Is fipronil safer than chlorpyrifos? Comparative developmental neurotoxicity modeled in PC12 cells.

Journal Article Brain Res Bull · March 30, 2009 Fipronil, a GABA(A) receptor antagonist, is replacing many insecticide uses formerly fulfilled by organophosphates like chlorpyrifos. Few studies have addressed the potential for fipronil to produce developmental neurotoxicity. We compared the neurotoxicit ... Full text Link to item Cite

Transcriptional profiles reveal similarities and differences in the effects of developmental neurotoxicants on differentiation into neurotransmitter phenotypes in PC12 cells.

Journal Article Brain Res Bull · March 16, 2009 Unrelated developmental neurotoxicants nevertheless converge on common functional and behavioral outcomes. We used PC12 cells, a model of neuronal development, to explore similarities and differences for organophosphate pesticides (chlorpyrifos, diazinon), ... Full text Link to item Cite

Ultraviolet photolysis of chlorpyrifos: developmental neurotoxicity modeled in PC12 cells.

Journal Article Environ Health Perspect · March 2009 BACKGROUND: Ultraviolet photodegradation products from pesticides form both in the field and during water treatment. OBJECTIVES: We evaluated the photolytic breakdown of the organophosphate pesticide chlorpyrifos (CPF) in terms of both the chemical entitie ... Full text Link to item Cite

Neonatal parathion exposure disrupts serotonin and dopamine synaptic function in rat brain regions: modulation by a high-fat diet in adulthood.

Journal Article Neurotoxicol Teratol · 2009 The consequences of exposure to developmental neurotoxicants are influenced by environmental factors. In the present study, we examined the role of dietary fat intake. We administered parathion to neonatal rats and then evaluated whether a high-fat diet be ... Full text Link to item Cite

Developmental neurotoxicity of parathion: progressive effects on serotonergic systems in adolescence and adulthood.

Journal Article Neurotoxicol Teratol · 2009 Neonatal exposures to organophosphates that are not acutely symptomatic or that produce little or no cholinesterase inhibition can nevertheless compromise the development and later function of critical neural pathways, including serotonin (5HT) systems tha ... Full text Link to item Cite

Neurobehavioral teratogenicity of sarin in an avian model.

Journal Article Neurotoxicol Teratol · 2009 Nerve gas organophosphates like sarin are likely to be used in urban terrorism, leading to widespread exposures of pregnant women and young children. Here, we established a model for sarin neurobehavioral teratogenicity in the developing chick so as to exp ... Full text Link to item Cite

Nicotine exposure in adolescence alters the response of serotonin systems to nicotine administered subsequently in adulthood.

Journal Article Dev Neurosci · 2009 Developmental nicotine exposure produces lasting changes in serotonin (5-HT) function. We gave nicotine to adolescent rats (postnatal days, PD, 30-47), simulating plasma levels in smokers, and then examined the subsequent effects of nicotine given again in ... Full text Link to item Cite

Nonenzymatic role of acetylcholinesterase in neuritic sprouting: regional changes in acetylcholinesterase and choline acetyltransferase after neonatal 6-hydroxydopamine lesions.

Journal Article Neurotoxicol Teratol · 2009 Acetylcholinesterase (AChE) is postulated to play a nonenzymatic role in the development of neuritic projections. We gave the specific neurotoxin, 6-OHDA to rats on postnatal day (PN) 1, a treatment that destroys noradrenergic nerve terminals in the forebr ... Full text Link to item Cite

Material tobacco smoking, nicotine replacement and neurobehavioural development (Acta Paediatrica, International Journal of Paediatrics (2008) 97, (1331-1337))

Journal Article Acta Paediatrica, International Journal of Paediatrics · January 1, 2009 Full text Cite

Transitioning Silver: From Big to Small, Safe to Unsafe?

Journal Article INTERNATIONAL JOURNAL OF TOXICOLOGY · January 1, 2009 Link to item Cite

Persistent behavioral alterations in rats neonatally exposed to low doses of the organophosphate pesticide, parathion.

Journal Article Brain Res Bull · December 16, 2008 Although developmental exposures of rats to low levels of the organophosphate pesticides (OPs), chlorpyrifos (CPF) or diazinon (DZN), both cause persistent neurobehavioral effects, there are important differences in their neurotoxicity. The current study e ... Full text Link to item Cite

Developmental neurotoxicants target neurodifferentiation into the serotonin phenotype: Chlorpyrifos, diazinon, dieldrin and divalent nickel.

Journal Article Toxicol Appl Pharmacol · December 1, 2008 Developmental exposure to organophosphates (OP) produces long-term changes in serotonin (5HT) synaptic function and associated behaviors, but there are disparities among the different OPs. We contrasted effects of chlorpyrifos and diazinon, as well as non- ... Full text Link to item Cite

Exposure of neonatal rats to parathion elicits sex-selective reprogramming of metabolism and alters the response to a high-fat diet in adulthood.

Journal Article Environ Health Perspect · November 2008 BACKGROUND: Developmental exposures to organophosphate pesticides are virtually ubiquitous. These agents are neurotoxicants, but recent evidence also points to lasting effects on metabolism. OBJECTIVES: We administered parathion to neonatal rats. In adulth ... Full text Link to item Cite

Exposure of neonatal rats to parathion elicits sex-selective impairment of acetylcholine systems in brain regions during adolescence and adulthood.

Journal Article Environ Health Perspect · October 2008 BACKGROUND: Organophosphates elicit developmental neurotoxicity through multiple mechanisms other than their shared property as cholinesterase inhibitors. Accordingly, these agents may differ in their effects on specific brain circuits. OBJECTIVES: We gave ... Full text Link to item Cite

Maternal tobacco smoking, nicotine replacement and neurobehavioural development.

Journal Article Acta Paediatr · October 2008 Abstract The adverse effects of prenatal cigarette smoke exposure on human reproductive outcomes are a major scientific and public health concern. In the United States, approximately 25% of women of childbearing age currently smoke cigarettes, and only a s ... Full text Link to item Cite

Adolescent nicotine administration changes the responses to nicotine given subsequently in adulthood: adenylyl cyclase cell signaling in brain regions during nicotine administration and withdrawal, and lasting effects.

Journal Article Brain Res Bull · July 30, 2008 Neurodevelopmental vulnerability to nicotine extends into adolescence, the stage at which most smokers begin using tobacco. The "sensitization-homeostasis" model postulates that nicotine treatment permanently reprogrammes neural communication, so that unde ... Full text Link to item Cite

Development of glucocorticoid receptor regulation in the rat forebrain: implications for adverse effects of glucocorticoids in preterm infants.

Journal Article Brain Res Bull · July 30, 2008 Glucocorticoids are the consensus treatment to avoid respiratory distress in preterm infants but there is accumulating evidence that these agents evoke long-term neurobehavioral deficits. Earlier, we showed that the developing rat forebrain is far more sen ... Full text Link to item Cite

Targeting of neurotrophic factors, their receptors, and signaling pathways in the developmental neurotoxicity of organophosphates in vivo and in vitro.

Journal Article Brain Res Bull · July 1, 2008 Neurotrophic factors control neural cell differentiation and assembly of neural circuits. We previously showed that organophosphate pesticides differentially regulate members of the fibroblast growth factor (fgf) gene family. We administered chlorpyrifos a ... Full text Link to item Cite

Developmental neurotoxicity of perfluorinated chemicals modeled in vitro.

Journal Article Environ Health Perspect · June 2008 BACKGROUND: The widespread detection of perfluoroalkyl acids and their derivatives in wildlife and humans, and their entry into the immature brain, raise increasing concern about whether these agents might be developmental neurotoxicants. OBJECTIVES: We ev ... Full text Link to item Cite

Adolescent nicotine treatment changes the response of acetylcholine systems to subsequent nicotine administration in adulthood.

Journal Article Brain Res Bull · May 15, 2008 Nicotine alters the developmental trajectory of acetylcholine (ACh) systems in the immature brain, with vulnerability extending from fetal stages through adolescence. We administered nicotine to adolescent rats (postnatal days PN30-47) and then examined th ... Full text Link to item Cite

Developmental neurotoxicity of low dose diazinon exposure of neonatal rats: effects on serotonin systems in adolescence and adulthood.

Journal Article Brain Res Bull · March 28, 2008 The developmental neurotoxicity of organophosphate pesticides targets serotonin (5HT) systems, which are involved in emotional and appetitive behaviors. We exposed neonatal rats to daily doses of diazinon on postnatal days 1-4, using doses (0.5 or 2mg/kg) ... Full text Link to item Cite

Neonatal exposure to low doses of diazinon: long-term effects on neural cell development and acetylcholine systems.

Journal Article Environ Health Perspect · March 2008 BACKGROUND: The developmental neurotoxicity of organophosphate pesticides involves mechanisms other than their shared property of cholinesterase inhibition. OBJECTIVES: We gave diazinon (DZN) to newborn rats on postnatal days 1-4, using doses (0.5 or 2 mg/ ... Full text Link to item Cite

Fetal mechanisms in neurodevelopmental disorders.

Journal Article Pediatr Neurol · March 2008 Normal development of the central nervous system depends on complex, dynamic mechanisms with multiple spatial and temporal components during gestation. Neurodevelopmental disorders may originate during fetal life from genetic as well as intrauterine and ex ... Full text Link to item Cite

Developmental diazinon neurotoxicity in rats: later effects on emotional response.

Journal Article Brain Res Bull · January 31, 2008 Developmental exposure to the organophosphorus pesticides chlorpyrifos and diazinon (DZN) alters serotonergic synaptic function at doses below the threshold for cholinesterase inhibition, however there are some indications that the two agents may differ in ... Full text Link to item Cite

Sea urchin embryonic development provides a model for evaluating therapies against beta-amyloid toxicity.

Journal Article Brain Res Bull · January 31, 2008 Accumulation of beta-amyloid protein is an Alzheimer's disease hallmark but also may be mechanistically involved in neurodegeneration. One of its cleavage peptides, Abeta42, has been used to evaluate the mechanisms underlying amyloid-induced cytotoxicity a ... Full text Link to item Cite

Persistent cognitive alterations in rats after early postnatal exposure to low doses of the organophosphate pesticide, diazinon.

Journal Article Neurotoxicol Teratol · 2008 BACKGROUND: Developmental neurotoxicity of organophosphorous insecticides (OPs) involves multiple mechanisms in addition to cholinesterase inhibition. We have found persisting effects of developmental chlorpyrifos (CPF) and diazinon (DZN) on cholinergic an ... Full text Link to item Cite

Amyloid precursor protein 96-110 and beta-amyloid 1-42 elicit developmental anomalies in sea urchin embryos and larvae that are alleviated by neurotransmitter analogs for acetylcholine, serotonin and cannabinoids.

Journal Article Neurotoxicol Teratol · 2008 Amyloid precursor protein (APP) is overexpressed in the developing brain and portions of its extracellular domain, especially amino acid residues 96-110, play an important role in neurite outgrowth and neural cell differentiation. In the current study, we ... Full text Link to item Cite

Developmental neurotoxic effects of chlorpyrifos on acetylcholine and serotonin pathways in an avian model.

Journal Article Neurotoxicol Teratol · 2008 The developmental neurotoxicity of organophosphates such as chlorpyrifos (CPF) involves multiple mechanisms that ultimately compromise the function of specific neurotransmitter systems, notably acetylcholine (ACh) and serotonin (5-hydroxytryptamine, 5HT). ... Full text Link to item Cite

Exposure of developing chicks to perfluorooctanoic acid induces defects in prehatch and early posthatch development.

Journal Article J Toxicol Environ Health A · 2008 There is increasing concern over the widespread use of perfluorinated chemicals, which accumulate in various tissues and penetrate the mammalian fetus. A chick model was established for the rapid evaluation of teratogenicity of these chemicals, an importan ... Full text Link to item Cite

If nicotine is a developmental neurotoxicant in animal studies, dare we recommend nicotine replacement therapy in pregnant women and adolescents?

Journal Article Neurotoxicol Teratol · 2008 Tobacco use in pregnancy is a leading cause of perinatal morbidity and contributes in major ways to attention deficit hyperactivity disorder, conduct disorders and learning disabilities that emerge in childhood and adolescence. Over the past two decades, a ... Full text Link to item Cite

Gender-specific effects of prenatal and adolescent exposure to tobacco smoke on auditory and visual attention.

Journal Article Neuropsychopharmacology · December 2007 Prenatal exposure to active maternal tobacco smoking elevates risk of cognitive and auditory processing deficits, and of smoking in offspring. Recent preclinical work has demonstrated a sex-specific pattern of reduction in cortical cholinergic markers foll ... Full text Link to item Cite

The sea urchin embryo, an invertebrate model for mammalian developmental neurotoxicity, reveals multiple neurotransmitter mechanisms for effects of chlorpyrifos: therapeutic interventions and a comparison with the monoamine depleter, reserpine.

Journal Article Brain Res Bull · September 28, 2007 Lower organisms show promise for the screening of neurotoxicants that might target mammalian brain development. Sea urchins use neurotransmitters as embryonic growth regulatory signals, so that adverse effects on neural substrates for mammalian brain devel ... Full text Link to item Cite

Separate or sequential exposure to nicotine prenatally and in adulthood: persistent effects on acetylcholine systems in rat brain regions.

Journal Article Brain Res Bull · September 14, 2007 Nicotine is a developmental neurotoxicant but the proposed "sensitization-homeostasis" model postulates that even in adulthood nicotine permanently reprograms synaptic function. We administered nicotine to rats throughout gestation or in adulthood (postnat ... Full text Link to item Cite

Ameliorating the developmental neurotoxicity of chlorpyrifos: a mechanisms-based approach in PC12 cells.

Journal Article Environ Health Perspect · September 2007 BACKGROUND: Organophosphate developmental neurotoxicity involves multiple mechanisms converging on neural cell replication and differentiation. OBJECTIVES: We evaluated mechanisms contributing to the adverse effects of chlorpyrifos (CPF) on DNA synthesis, ... Full text Link to item Cite

Developmental exposure to terbutaline and chlorpyrifos, separately or sequentially, elicits presynaptic serotonergic hyperactivity in juvenile and adolescent rats.

Journal Article Brain Res Bull · July 12, 2007 Developmental exposure to unrelated neurotoxicants can nevertheless converge on common final targets so as to exacerbate damage or functional deficits. We examined the effects of developmental exposure to terbutaline, a beta2-adrenergic receptor agonist us ... Full text Link to item Cite

Lasting effects of nicotine treatment and withdrawal on serotonergic systems and cell signaling in rat brain regions: separate or sequential exposure during fetal development and adulthood.

Journal Article Brain Res Bull · July 12, 2007 Neurodevelopmental vulnerability to nicotine extends from fetal stages through adolescence. The recently proposed "sensitization-homeostasis" model postulates that, even in adulthood, nicotine treatment permanently reprograms synaptic activity. We administ ... Full text Link to item Cite

Neuroinflammation and behavioral abnormalities after neonatal terbutaline treatment in rats: implications for autism.

Journal Article J Pharmacol Exp Ther · July 2007 Autism is a neurodevelopmental disorder presenting before 3 years of age with deficits in communication and social skills and repetitive behaviors. In addition to genetic influences, recent studies suggest that prenatal drug or chemical exposures are risk ... Full text Link to item Cite

Visual recognition memory and auditory brainstem response in infant rhesus monkeys exposed perinatally to environmental tobacco smoke.

Journal Article Brain Res · June 2, 2007 The impact of perinatal exposure to environmental tobacco smoke (ETS) on cognitive development is controversial. We exposed rhesus monkeys to ETS or filtered air (5 animals per group) beginning in utero on day 50 of pregnancy and continuing throughout post ... Full text Link to item Cite

Exposure to organophosphates reduces the expression of neurotrophic factors in neonatal rat brain regions: similarities and differences in the effects of chlorpyrifos and diazinon on the fibroblast growth factor superfamily.

Journal Article Environ Health Perspect · June 2007 BACKGROUND: The fibroblast growth factor (FGF) superfamily of neurotrophic factors plays critical roles in neural cell development, brain assembly, and recovery from neuronal injury. OBJECTIVES: We administered two organophosphate pesticides, chlorpyrifos ... Full text Link to item Cite

Comparative developmental neurotoxicity of organophosphates in vivo: transcriptional responses of pathways for brain cell development, cell signaling, cytotoxicity and neurotransmitter systems.

Journal Article Brain Res Bull · May 30, 2007 Organophosphates affect mammalian brain development through a variety of mechanisms beyond their shared property of cholinesterase inhibition. We used microarrays to characterize similarities and differences in transcriptional responses to chlorpyrifos and ... Full text Link to item Cite

Permanent, sex-selective effects of prenatal or adolescent nicotine exposure, separately or sequentially, in rat brain regions: indices of cholinergic and serotonergic synaptic function, cell signaling, and neural cell number and size at 6 months of age.

Journal Article Neuropsychopharmacology · May 2007 Nicotine is a neuroteratogen that disrupts neurodevelopment and synaptic function, with vulnerability extending into adolescence. We assessed the permanence of effects in rats on indices of neural cell number and size, and on acetylcholine and serotonin (5 ... Full text Link to item Cite

Complementary zebrafish and rat models of developmental neurobehavioral toxicity: The case of organophosphate pesticide exposure

Conference Neurotoxicology and Teratology · May 2007 Full text Cite

If nicotine is a developmental neurotoxicant in animal studies, dare we recommend nicotine replacement therapy in pregnant women and adolescents?

Conference Neurotoxicology and Teratology · May 2007 Full text Cite

Critical review: nicotine for the fetus, the infant and the adolescent?

Journal Article J Health Psychol · March 2007 The recent expansion of Nicotine Replacement Therapy to pregnant women and children ignores the fact that nicotine impairs, disrupts, duplicates and/or interacts with essential physiological functions and is involved in tobacco-related carcinogenesis. The ... Full text Link to item Cite

A unique role for striatal serotonergic systems in the withdrawal from adolescent nicotine administration.

Journal Article Neurotoxicol Teratol · 2007 Adolescent smokers experience more severe withdrawal symptoms upon smoking cessation than do adults, even when daily smoking has occurred for only a short period or with low levels of consumption. Animal models of nicotine withdrawal indicate involvement o ... Full text Link to item Cite

Nonenzymatic functions of acetylcholinesterase splice variants in the developmental neurotoxicity of organophosphates: chlorpyrifos, chlorpyrifos oxon, and diazinon.

Journal Article Environ Health Perspect · January 2007 BACKGROUND: Organophosphate pesticides affect mammalian brain development through mechanisms separable from the inhibition of acetylcholinesterase (AChE) enzymatic activity and resultant cholinergic hyperstimulation. In the brain, AChE has two catalyticall ... Full text Link to item Cite

Screening for developmental neurotoxicity using PC12 cells: comparisons of organophosphates with a carbamate, an organochlorine, and divalent nickel.

Journal Article Environ Health Perspect · January 2007 BACKGROUND: In light of the large number of chemicals that are potential developmental neurotoxicants, there is a need to develop rapid screening techniques. OBJECTIVES: We exposed undifferentiated and differentiating neuronotypic PC12 cells to different o ... Full text Link to item Cite

Adolescent vs. adult-onset nicotine self-administration in male rats: duration of effect and differential nicotinic receptor correlates.

Journal Article Neurotoxicol Teratol · 2007 Adolescence is the life stage when tobacco addiction typically begins. Adolescent neurobehavioral development may be altered by nicotine self-administration in a way that persistently potentiates addiction. Previously, we showed that female adolescent rats ... Full text Link to item Cite

Prenatal chlorpyrifos exposure elicits presynaptic serotonergic and dopaminergic hyperactivity at adolescence: critical periods for regional and sex-selective effects.

Journal Article Reprod Toxicol · 2007 Fetal or neonatal chlorpyrifos (CPF) exposure affects serotonin (5HT) synaptic function and related behaviors in adulthood. We examined the critical period and dose threshold for effects on 5HT and assessed their emergence in adolescence. Pregnant rats wer ... Full text Link to item Cite

Low dose early postnatal diazinon exposure causes impaired working memory on the radial-arm maze in rats during adulthood.

Conference NEUROTOXICOLOGY · December 1, 2006 Link to item Cite

Are nonenzymatic functions of acetylcholinesterase (AChE) involved in the developmental neurotoxicity of organophosphates? Effects of chlorpyrifos and diazinon on expression of AChE splice variants in vitro and in vivo.

Conference NEUROTOXICOLOGY · December 1, 2006 Link to item Cite

Developmental neurotoxicity of organophosphates: a case study of chlorpyrifos

Journal Article · December 1, 2006 The chapter addresses the case of chlorpyrifos as a specific example of how knowledge of the systemic toxicity of an organophosphate in adults can be misleading with regard to its potential to act as a developmental neurotoxicant. A case study of the devel ... Full text Cite

Prenatal nicotine exposure alters the responses to subsequent nicotine administration and withdrawal in adolescence: Serotonin receptors and cell signaling.

Journal Article Neuropsychopharmacology · November 2006 Offspring of women who smoke during pregnancy are themselves more likely to take up smoking in adolescence, effects that are associated with a high rate of depression and increased sensitivity to withdrawal symptoms. To evaluate the biological basis for th ... Full text Link to item Cite

Increased nicotine self-administration following prenatal exposure in female rats.

Journal Article Pharmacol Biochem Behav · November 2006 There is a significant association between maternal cigarette smoking during pregnancy and greater subsequent risk of smoking in female offspring. In animal models, prenatal nicotine exposure causes persistent alterations in cholinergic and monoaminergic s ... Full text Link to item Cite

Persisting effects of early postnatal diazinon exposure on emotional reactivity in rats

Conference Neurotoxicology and Teratology · November 2006 Full text Cite

Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition.

Journal Article Environ Health Perspect · October 2006 BACKGROUND: In the developing brain, serotonin (5HT) systems are among the most sensitive to disruption by organophosphates. OBJECTIVES: We exposed neonatal rats to daily doses of diazinon or parathion on postnatal days (PND)1-4 and evaluated 5HT receptors ... Full text Link to item Cite

Alterations of serotonin synaptic proteins in brain regions of neonatal Rhesus monkeys exposed to perinatal environmental tobacco smoke.

Journal Article Brain Res · September 21, 2006 Serotonin (5HT) systems play important roles in brain development, and early perturbations of 5HT receptor expression produce permanent changes in 5HT synaptic function and associated behaviors. We exposed pregnant Rhesus monkeys to environmental tobacco s ... Full text Link to item Cite

Chlorpyrifos affects neuronal cell replication and phenotypic outcomes.

Conference NEUROTOXICOLOGY · September 1, 2006 Link to item Cite

Adverse neurodevelopmental effects of dexamethasone modeled in PC12 cells: identifying the critical stages and concentration thresholds for the targeting of cell acquisition, differentiation and viability.

Journal Article Neuropsychopharmacology · August 2006 The use of dexamethasone (DEX) to prevent respiratory distress in preterm infants is suspected to produce neurobehavioral deficits. We used PC12 cells to model the effects of DEX on different stages of neuronal development, utilizing exposures from 24 h up ... Full text Link to item Cite

Visuospatial memory deficits emerging during nicotine withdrawal in adolescents with prenatal exposure to active maternal smoking.

Journal Article Neuropsychopharmacology · July 2006 Active maternal smoking during pregnancy elevates the risk of cognitive deficits and tobacco smoking among offspring. Preclinical work has shown that combined prenatal and adolescent exposure to nicotine produces more pronounced hippocampal changes and gre ... Full text Link to item Cite

Critical prenatal and postnatal periods for persistent effects of dexamethasone on serotonergic and dopaminergic systems.

Journal Article Neuropsychopharmacology · May 2006 Glucocorticoid administration to preterm infants is associated with neurodevelopmental disorders. We treated developing rats with dexamethasone (Dex) at 0.05, 0.2, or 0.8 mg/kg, doses below or spanning the range in clinical use, testing the effects of admi ... Full text Link to item Cite

Chlorpyrifos affects phenotypic outcomes in a model of mammalian neurodevelopment: critical stages targeting differentiation in PC12 cells.

Journal Article Environ Health Perspect · May 2006 The organophosphate insecticide chlorpyrifos (CPF) adversely affects mammalian brain development through multiple mechanisms. To determine if CPF directly affects neuronal cell replication and phenotypic fate, and to identify the vulnerable stages of diffe ... Full text Link to item Cite

Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity.

Journal Article Environ Health Perspect · May 2006 A comparative approach to the differences between systemic toxicity and developmental neurotoxicity of organophosphates is critical to determine the degree to which multiple mechanisms of toxicity carry across different members of this class of insecticide ... Full text Link to item Cite

Anomalous regulation of beta-adrenoceptor signaling in brain regions of the newborn rat.

Journal Article Brain Res · March 10, 2006 Desensitization, an essential homeostatic response to excessive or continued beta-adrenoceptor (betaAR) stimulation, is deficient in immature cells. To determine the mechanisms underlying anomalous betaAR responses in newborn rats, we administered terbutal ... Full text Link to item Cite

Cholinergic receptor subtypes in the olfactory bulbectomy model of depression.

Journal Article Brain Res Bull · January 30, 2006 The connection between smoking and depression, the antidepressant actions of nicotine and the targeting of nicotinic acetylcholine receptors (nAChRs) by monoamine re-uptake inhibitors all point to a potential role of nAChRs in the etiology and/or symptomat ... Full text Link to item Cite

Lasting effects of developmental dexamethasone treatment on neural cell number and size, synaptic activity, and cell signaling: critical periods of vulnerability, dose-effect relationships, regional targets, and sex selectivity.

Journal Article Neuropsychopharmacology · January 2006 Glucocorticoids administered to prevent respiratory distress in preterm infants are associated with neurodevelopmental disorders. To evaluate the long-term effects on forebrain development, we treated developing rats with dexamethasone (Dex) at 0.05, 0.2, ... Full text Link to item Cite

Perinatal environmental tobacco smoke exposure in rhesus monkeys: critical periods and regional selectivity for effects on brain cell development and lipid peroxidation.

Journal Article Environ Health Perspect · January 2006 Perinatal environmental tobacco smoke (ETS) exposure in humans elicits neurobehavioral deficits. We exposed rhesus monkeys to ETS during gestation and through 13 months postnatally, or postnatally only (6-13 months). At the conclusion of exposure, we exami ... Full text Link to item Cite

New perspectives on roles for neurotransmitters in early ("Pre-nervous") embryogenesis

Conference NEUROBIOLOGICAL STUDIES - FROM GENES TO BEHAVIOUR 2006 · January 1, 2006 Link to item Cite

Developmental Neurotoxicity of Organophosphates: A Case Study of Chlorpyrifos

Chapter · December 13, 2005 The chapter addresses the case of chlorpyrifos as a specific example of how knowledge of the systemic toxicity of an organophosphate in adults can be misleading with regard to its potential to act as a developmental neurotoxicant. A case study of the devel ... Full text Cite

Imbalances emerge in cardiac autonomic cell signaling after neonatal exposure to terbutaline or chlorpyrifos, alone or in combination.

Journal Article Brain Res Dev Brain Res · December 7, 2005 During early neonatal development, the future reactivity of the heart to cardiac autonomic stimulation is programmed by the timing and intensity of the arrival of parasympathetic and sympathetic inputs. In neonatal rats, we examined the effects of exposure ... Full text Link to item Cite

Prenatal stress elicits regionally selective changes in basal FGF-2 gene expression in adulthood and alters the adult response to acute or chronic stress.

Journal Article Neurobiol Dis · December 2005 Exposure to stress during pregnancy influences the trajectory of brain development resulting in permanent alterations that may contribute to increased susceptibility to subsequent cognitive or neuropsychiatric disorders. In this manuscript, we examined the ... Full text Link to item Cite

Disruption of rat forebrain development by glucocorticoids: critical perinatal periods for effects on neural cell acquisition and on cell signaling cascades mediating noradrenergic and cholinergic neurotransmitter/neurotrophic responses.

Journal Article Neuropsychopharmacology · October 2005 Glucocorticoids are the consensus treatment for the prevention of respiratory distress in preterm infants, but there is evidence for increased incidence of neurodevelopmental disorders as a result of their administration. We administered dexamethasone (Dex ... Full text Link to item Cite

Developmental exposure of rats to chlorpyrifos elicits sex-selective hyperlipidemia and hyperinsulinemia in adulthood.

Journal Article Environ Health Perspect · October 2005 Developmental exposure to chlorpyrifos alters cell signaling both in the brain and in peripheral tissues, affecting the responses to a variety of neurotransmitters and hormones. We administered 1 mg/kg/day chlorpyrifos to rats on postnatal days 1-4, a regi ... Full text Link to item Cite

Gestational dexamethasone treatment elicits sex-dependent alterations in locomotor activity, reward-based memory and hippocampal cholinergic function in adolescent and adult rats.

Journal Article Neuropsychopharmacology · September 2005 Glucocorticoids are the consensus treatment for preventing respiratory distress syndrome in preterm infants but there is emerging evidence of subsequent neurobehavioral abnormalities, independent of somatic growth effects. Pregnant rats were given 0.2 mg/k ... Full text Link to item Cite

The alterations in CNS serotonergic mechanisms caused by neonatal chlorpyrifos exposure are permanent.

Journal Article Brain Res Dev Brain Res · August 8, 2005 Fetal or neonatal exposure to chlorpyrifos (CPF) or related organophosphate pesticides leads to abnormalities of brain cell development, synaptic function, and behavior. Recent studies in rats indicate profound effects on serotonin (5HT) systems that origi ... Full text Link to item Cite

Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure.

Journal Article Environ Health Perspect · August 2005 Exposure to chlorpyrifos (CPF) alters neuronal development of serotonin (5HT) and dopamine systems, and we recently found long-term alterations in behaviors related to 5HT function. To characterize the synaptic mechanisms underlying these effects, we expos ... Full text Link to item Cite

Oxidative mechanisms contributing to the developmental neurotoxicity of nicotine and chlorpyrifos.

Journal Article Toxicol Appl Pharmacol · August 1, 2005 Nicotine and chlorpyrifos are developmental neurotoxicants that, despite their differences in structure and mechanism of action, share many aspects for damage to the developing brain. Both are thought to generate oxidative radicals; in the current study, w ... Full text Link to item Cite

Critical periods for the role of oxidative stress in the developmental neurotoxicity of chlorpyrifos and terbutaline, alone or in combination.

Journal Article Brain Res Dev Brain Res · June 30, 2005 The developmental neurotoxicity of chlorpyrifos (CPF) involves mechanisms other than inhibition of cholinesterase. In the current study, we examined the ability of CPF to evoke lipid peroxidation in the developing brain of fetal and neonatal rats. CPF give ... Full text Link to item Cite

Developmental exposure of rats to chlorpyrifos leads to behavioral alterations in adulthood, involving serotonergic mechanisms and resembling animal models of depression.

Journal Article Environ Health Perspect · May 2005 Developmental exposure to chlorpyrifos (CPF) causes persistent changes in serotonergic (5HT) systems. We administered 1 mg/kg/day CPF to rats on postnatal days 1-4, a regimen below the threshold for systemic toxicity. When tested in adulthood, CPF-exposed ... Full text Link to item Cite

Developmental neurotoxicity of chlorpyrifos: targeting glial cells.

Journal Article Environ Toxicol Pharmacol · May 2005 The pesticide chlorpyrifos (CPF) causes neurobehavioral damage, even at doses that do not elicit acute cholinergic toxicity. CPF disrupts the developing brain during glial proliferation and differentiation. Since glial cells play critical roles in brain de ... Full text Link to item Cite

Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats.

Journal Article Brain Res Dev Brain Res · March 22, 2005 Neurochemical and behavioral studies indicate that the widely used organophosphorus insecticide, chlorpyrifos (CPF), evokes neurobehavioral teratogenicity with a wide window of vulnerability, ranging from embryonic life through postnatal development. Few s ... Full text Link to item Cite

Developmental exposure to terbutaline alters cell signaling in mature rat brain regions and augments the effects of subsequent neonatal exposure to the organophosphorus insecticide chlorpyrifos.

Journal Article Toxicol Appl Pharmacol · March 1, 2005 Exposure to apparently unrelated neurotoxicants can nevertheless converge on common neurodevelopmental events. We examined the long-term effects of developmental exposure of rats to terbutaline, a beta-adrenoceptor agonist used to arrest preterm labor, and ... Full text Link to item Cite

Developmental exposure to terbutaline and chlorpyrifos: pharmacotherapy of preterm labor and an environmental neurotoxicant converge on serotonergic systems in neonatal rat brain regions.

Journal Article Toxicol Appl Pharmacol · March 1, 2005 Developmental exposure to unrelated neurotoxicants can nevertheless produce similar neurobehavioral outcomes. We examined the effects of developmental exposure to terbutaline, a tocolytic beta2-adrenoceptor agonist used to arrest preterm labor, and chlorpy ... Full text Link to item Cite

Modeling the developmental neurotoxicity of nicotine in vitro: cell acquisition, growth and viability in PC12 cells.

Journal Article Brain Res Dev Brain Res · February 8, 2005 Although nicotine is a developmental neurotoxicant, it also can exert neuroprotective effects. In the current study, we used PC12 cells to determine the developmental phases in which these disparate actions are expressed and to compare the concentrations r ... Full text Link to item Cite

Serotonergic cell signaling in an animal model of aging and depression: olfactory bulbectomy elicits different adaptations in brain regions of young adult vs aging rats.

Journal Article Neuropsychopharmacology · January 2005 Aging involves neuronal and synaptic loss, and maintenance of function depends on adaptations in cellular responsiveness. We studied olfactory bulbectomy (OBX), a model that recapitulates monoaminergic dysfunction in depression, in 10-week vs 19-month-old ... Full text Link to item Cite

Effects of prenatal nicotine exposure on primate brain development and attempted amelioration with supplemental choline or vitamin C: neurotransmitter receptors, cell signaling and cell development biomarkers in fetal brain regions of rhesus monkeys.

Journal Article Neuropsychopharmacology · January 2005 Studies in developing rodents indicate that nicotine is a neuroteratogen that disrupts brain development by stimulating nicotinic acetylcholine receptors (nAChRs) that control neural cell replication and differentiation. We administered nicotine to pregnan ... Full text Link to item Cite

Nicotine therapy in adulthood reverses the synaptic and behavioral deficits elicited by prenatal exposure to phenobarbital.

Journal Article Neuropsychopharmacology · January 2005 A major objective in identifying the mechanisms underlying neurobehavioral teratogenicity is the possibility of designing therapies that reverse or offset drug- or toxicant-induced neural damage. In our previous studies, we identified deficits in hippocamp ... Full text Link to item Cite

Mode of action: disruption of brain cell replication, second messenger, and neurotransmitter systems during development leading to cognitive dysfunction--developmental neurotoxicity of nicotine.

Journal Article Crit Rev Toxicol · 2005 Developmental exposure to nicotine in rats results in neurobehavioral effects such as reduced locomotor and cognitive function. Key events in the animal mode of action (MOA) include binding to the nicotinic cholinergic receptor during prenatal and/or early ... Full text Link to item Cite

Administration of nicotine to adolescent rats evokes regionally selective upregulation of CNS alpha 7 nicotinic acetylcholine receptors.

Journal Article Brain Res · December 24, 2004 Alpha 7 Nicotinic acetylcholine receptors (nAChRs) play a role in axonogenesis, synaptogenesis and synaptic plasticity, and are therefore targets for developmental neurotoxicants. We administered nicotine to adolescent rats and evaluated the effects on alp ... Full text Link to item Cite

Cholinergic synaptic signaling mechanisms underlying behavioral teratogenicity: effects of nicotine, chlorpyrifos, and heroin converge on protein kinase C translocation in the intermedial part of the hyperstriatum ventrale and on imprinting behavior in an avian model.

Journal Article J Neurosci Res · November 15, 2004 A wide variety of otherwise unrelated neuroteratogens elicit a common set of behavioral defects centering around cholinergic contributions to cognitive function. We utilized the developing chick to overcome confounds related to maternal effects and compare ... Full text Link to item Cite

Convergent effects on cell signaling mechanisms mediate the actions of different neurobehavioral teratogens: alterations in cholinergic regulation of protein kinase C in chick and avian models.

Journal Article Ann N Y Acad Sci · October 2004 Although the actions of heroin on central nervous system (CNS) development are mediated through opioid receptors, the net effects converge on dysfunction of cholinergic systems. We explored the mechanisms underlying neurobehavioral deficits in mouse and av ... Full text Link to item Cite

Alpha7 nicotinic acetylcholine receptors targeted by cholinergic developmental neurotoxicants: nicotine and chlorpyrifos.

Journal Article Brain Res Bull · September 30, 2004 Alpha7 nicotinic acetylcholine receptors (nAChRs) play a role in axonogenesis, synaptogenesis and synaptic plasticity, and are therefore potential targets for developmental neurotoxicants. We administered nicotine to neonatal rats during discrete periods s ... Full text Link to item Cite

Transiently overexpressed alpha2-adrenoceptors and their control of DNA synthesis in the developing brain.

Journal Article Brain Res Dev Brain Res · September 17, 2004 During brain development, neurotransmitters act as trophic factors controlling the patterns of cell replication and differentiation. Alpha2-adrenoceptors (alpha2ARs) are transiently overexpressed in zones with high mitotic activity and we evaluated whether ... Full text Link to item Cite

Does prenatal nicotine exposure sensitize the brain to nicotine-induced neurotoxicity in adolescence?

Journal Article Neuropsychopharmacology · August 2004 Offspring of women who smoke during pregnancy are themselves more likely to take up smoking in adolescence. We evaluated neurotoxicant effects of prenatal and adolescent nicotine exposure in developing rats to evaluate whether these contribute to a biologi ... Full text Link to item Cite

Cholinergic systems in brain development and disruption by neurotoxicants: nicotine, environmental tobacco smoke, organophosphates.

Journal Article Toxicol Appl Pharmacol · July 15, 2004 Acetylcholine and other neurotransmitters play unique trophic roles in brain development. Accordingly, drugs and environmental toxicants that promote or interfere with neurotransmitter function evoke neurodevelopmental abnormalities by disrupting the timin ... Full text Link to item Cite

Guidelines for developmental neurotoxicity and their impact on organophosphate pesticides: a personal view from an academic perspective.

Journal Article Neurotoxicology · June 2004 The appropriate regulation of drugs, chemicals and environmental contaminants requires the establishment of clear and accepted guidelines for developmental neurotoxicity. Ideally, these guidelines should encompass the ability to assess widely disparate cla ... Full text Link to item Cite

Prenatal nicotine exposure alters the response to nicotine administration in adolescence: effects on cholinergic systems during exposure and withdrawal.

Journal Article Neuropsychopharmacology · May 2004 Maternal smoking during pregnancy increases the likelihood that the offspring will become smokers in adolescence. In the current study, we evaluated effects of prenatal and adolescent nicotine exposure in rats to assess whether there is a biological basis ... Full text Link to item Cite

Critical periods for chlorpyrifos-induced developmental neurotoxicity: alterations in adenylyl cyclase signaling in adult rat brain regions after gestational or neonatal exposure.

Journal Article Environ Health Perspect · March 2004 Developmental exposure to chlorpyrifos (CPF) alters the function of a wide variety of neural systems. In the present study we evaluated the effects in adulthood of CPF exposure of rats during different developmental windows, using the adenylyl cyclase (AC) ... Full text Link to item Cite

Does pharmacotherapy for preterm labor sensitize the developing brain to environmental neurotoxicants? Cellular and synaptic effects of sequential exposure to terbutaline and chlorpyrifos in neonatal rats.

Journal Article Toxicol Appl Pharmacol · March 1, 2004 It is increasingly clear that environmental toxicants target specific human subpopulations. In the current study, we examined the effects of prior developmental exposure to a beta(2)-adrenoceptor agonist used to arrest preterm labor, terbutaline, on the su ... Full text Link to item Cite

Altered localization of choline transporter sites in the mouse hippocampus after prenatal heroin exposure.

Journal Article Brain Res Bull · March 1, 2004 Prenatal heroin exposure disrupts hippocampal cholinergic synaptic function and related behaviors. Biochemical studies indicate an increase in the number of presynaptic high-affinity choline transporter (HACT) sites, as assessed by [3H]hemicholinium-3 (HC- ... Full text Link to item Cite

Morphologic effects of subtoxic neonatal chlorpyrifos exposure in developing rat brain: regionally selective alterations in neurons and glia.

Journal Article Brain Res Dev Brain Res · February 20, 2004 The widely used organophosphate insecticide, chlorpyrifos (CPF), elicits neurobehavioral teratogenesis with exposure windows ranging from the embryonic neural tube stage through postnatal development. To explore the morphologic changes occurring in late-st ... Full text Link to item Cite

Terbutaline is a developmental neurotoxicant: effects on neuroproteins and morphology in cerebellum, hippocampus, and somatosensory cortex.

Journal Article J Pharmacol Exp Ther · February 2004 Beta(2)-adrenoceptor agonists, especially terbutaline, are widely used to arrest preterm labor, but they also cross the placenta to stimulate fetal beta-adrenoceptors that control neural cell differentiation. We evaluated the effects of terbutaline adminis ... Full text Link to item Cite

Developmental effects of chlorpyrifos extend beyond neurotoxicity: critical periods for immediate and delayed-onset effects on cardiac and hepatic cell signaling.

Journal Article Environ Health Perspect · February 2004 The fetal and neonatal neurotoxicity of chlorpyrifos (CPF) and related insecticides is a major concern. Developmental effects of CPF involve mechanisms over and above cholinesterase inhibition, notably events in cell signaling that are shared by nonneural ... Full text Link to item Cite

Developmental exposure to chlorpyrifos elicits sex-selective alterations of serotonergic synaptic function in adulthood: critical periods and regional selectivity for effects on the serotonin transporter, receptor subtypes, and cell signaling.

Journal Article Environ Health Perspect · February 2004 During brain development, serotonin (5HT) provides essential neurotrophic signals, and in earlier work, we found that developmental exposure to chlorpyrifos (CPF) elicits short-term changes in 5HT systems. In the present study, we evaluated the effects in ... Full text Link to item Cite

Chlorpyrifos exposure during neurulation: cholinergic synaptic dysfunction and cellular alterations in brain regions at adolescence and adulthood.

Journal Article Brain Res Dev Brain Res · January 31, 2004 The developmental neurotoxicity of chlorpyrifos (CPF) involves multiple mechanisms, thus rendering the immature brain susceptible to adverse effects over a wide window of vulnerability. Earlier work indicated that CPF exposure at the neural tube stage elic ... Full text Link to item Cite

Beta-adrenoceptor modulation of transiently overexpressed alpha 2-adrenoceptors in brain and peripheral tissues: cellular mechanisms underlying the developmental toxicity of terbutaline.

Journal Article Brain Res Bull · January 15, 2004 Terbutaline, a selective beta(2)-adrenoceptor (beta(2)AR) agonist, is widely used as a tocolytic to arrest preterm labor but recent studies indicate that excessive betaAR stimulation can alter the expression and function of other neurotransmitter receptors ... Full text Link to item Cite

Behavioral alterations in adolescent and adult rats caused by a brief subtoxic exposure to chlorpyrifos during neurulation.

Journal Article Neurotoxicol Teratol · 2004 The widely used organophosphate insecticide, chlorpyrifos (CPF), elicits neurobehavioral abnormalities after apparently subtoxic neonatal exposures. In the current study, we administered 1 or 5 mg/kg/day of CPF to pregnant rats on gestational days 9-12, th ... Full text Link to item Cite

Nicotine is a developmental neurotoxicant and neuroprotectant: stage-selective inhibition of DNA synthesis coincident with shielding from effects of chlorpyrifos.

Journal Article Brain Res Dev Brain Res · December 30, 2003 Although nicotine is now well recognized as a developmental neurotoxicant, it also may have neuroprotectant properties. In the current study, we used PC12 cells to characterize the specific developmental phases in which these effects are expressed. In undi ... Full text Link to item Cite

Developmental neurotoxicity elicited by gestational exposure to chlorpyrifos: when is adenylyl cyclase a target?

Journal Article Environ Health Perspect · December 2003 The developmental neurotoxicity of chlorpyrifos (CPF) involves mechanisms over and above cholinesterase inhibition. In the present study, we evaluated the effects of gestational CPF exposure on the adenylyl cyclase (AC) signaling cascade, which regulates t ... Full text Link to item Cite

Short-term adolescent nicotine exposure in rats elicits immediate and delayed deficits in T-lymphocyte function: critical periods, patterns of exposure, dose thresholds.

Journal Article Nicotine Tob Res · December 2003 Prenatal nicotine exposure elicits lasting deficiencies in T-lymphocyte mitogenesis, and the period of vulnerability extends into adolescence, the stage at which smoking typically commences. We explored the importance of nicotine exposure patterns (continu ... Full text Link to item Cite

Does terbutaline damage the developing heart?

Journal Article Birth Defects Res B Dev Reprod Toxicol · December 2003 BACKGROUND: Beta(2)-Adrenoceptor (betaAR) agonists, such as terbutaline, are widely used to arrest preterm labor. They also cross the placenta where they stimulate receptors in fetal tissues, which in turn use betaAR input for trophic control of cell repli ... Full text Link to item Cite

Sex-selective hippocampal alterations after adolescent nicotine administration: effects on neurospecific proteins.

Journal Article Nicotine Tob Res · December 2003 Nicotine is a neuroteratogen that targets cell development and synaptic function into adolescence, when smoking typically commences. We used a rat model of adolescent nicotine exposure to characterize the types of cells involved in hippocampal alterations. ... Full text Link to item Cite

Short-term adolescent nicotine exposure has immediate and persistent effects on cholinergic systems: critical periods, patterns of exposure, dose thresholds.

Journal Article Neuropsychopharmacology · November 2003 In adolescents, the symptoms of nicotine dependence can appear well before the onset of habitual smoking. We investigated short-term nicotine exposure in adolescent rats for corresponding cholinergic alterations. Beginning on postnatal day 30, rats were gi ... Full text Link to item Cite

Serotonergic systems targeted by developmental exposure to chlorpyrifos: effects during different critical periods.

Journal Article Environ Health Perspect · November 2003 During brain development, serotonin (5HT) provides essential neurotrophic signals. In the present study, we evaluated whether the developmental neurotoxicity of chlorpyrifos (CPF) involves effects on 5HT signaling, as a potential mechanism underlying nonch ... Full text Link to item Cite

The sea urchin embryo as a model for mammalian developmental neurotoxicity: ontogenesis of the high-affinity choline transporter and its role in cholinergic trophic activity.

Journal Article Environ Health Perspect · November 2003 Embryonic development in the sea urchin requires trophic actions of the same neurotransmitters that participate in mammalian brain assembly. We evaluated the development of the high-affinity choline transporter, which controls acetylcholine synthesis. A va ... Full text Link to item Cite

Impact of adolescent nicotine exposure on adenylyl cyclase-mediated cell signaling: enzyme induction, neurotransmitter-specific effects, regional selectivities, and the role of withdrawal.

Journal Article Brain Res · October 24, 2003 Recent animal studies indicate that the adolescent brain is especially vulnerable to nicotine-induced alterations in synaptic function, echoing the increased susceptibility to nicotine dependence and withdrawal noted for adolescent smokers. We administered ... Full text Link to item Cite

Heroin neuroteratogenicity: delayed-onset deficits in catecholaminergic synaptic activity.

Journal Article Brain Res · September 12, 2003 Prenatal heroin exposure evokes neurochemical and behavioral deficits that, in part, reflect disruption of septohippocampal cholinergic function. In earlier studies, we found that cholinergic synaptic defects involve primary changes in cell signaling prote ... Full text Link to item Cite

Long-lasting CNS effects of a short-term chemical knockout of ornithine decarboxylase during development: nicotinic cholinergic receptor upregulation and subtle macromolecular changes in adulthood.

Journal Article Brain Res · August 15, 2003 Ornithine decarboxylase (ODC) and the polyamines play an essential role in brain cell replication and differentiation and polyamines also regulate the function of nicotinic acetylcholine receptors (nAChRs). We administered alpha-difluoromethylornithine (DF ... Full text Link to item Cite

Nicotine is a neurotoxin in the adolescent brain: critical periods, patterns of exposure, regional selectivity, and dose thresholds for macromolecular alterations.

Journal Article Brain Res · July 25, 2003 In the fetus, nicotine is a neuroteratogen that elicits cell damage and loss and subsequent abnormalities of synaptic function. We explored whether these effects extend into adolescence, the period when most people begin smoking. Beginning on postnatal day ... Full text Link to item Cite

Ontogenesis of beta-adrenoceptor signaling: implications for perinatal physiology and for fetal effects of tocolytic drugs.

Journal Article J Pharmacol Exp Ther · July 2003 G-Protein-coupled receptors play an instrumental role in cellular development and function. In the mature organism, receptor signaling is controlled through the processes of desensitization and down-regulation. Recent evidence suggests that these regulator ... Full text Link to item Cite

Fetal chlorpyrifos exposure: adverse effects on brain cell development and cholinergic biomarkers emerge postnatally and continue into adolescence and adulthood.

Journal Article Environ Health Perspect · April 2003 Fetal and childhood exposures to widely used organophosphate pesticides, especially chlorpyrifos (CPF), have raised concerns about developmental neurotoxicity. Previously, biomarkers for brain cell number, cell packing density, and cell size indicated that ... Full text Link to item Cite

Neonatal chlorpyrifos exposure: Regionally-selective alterations in neuronal cell dimensions and in the number of neurons and glia in developing rat brain

Conference FASEB JOURNAL · March 14, 2003 Link to item Cite

Developmental neurotoxicity elicited by prenatal or postnatal chlorpyrifos exposure: effects on neurospecific proteins indicate changing vulnerabilities.

Journal Article Environ Health Perspect · March 2003 The developmental neurotoxicity of the organophosphate pesticide chlorpyrifos (CPF) is thought to involve both neurons and glia, thus producing a prolonged window of vulnerability. To characterize the cell types and brain regions involved in these effects, ... Full text Link to item Cite

Adolescent nicotine elicits glial and neuronal damage in rat brain

Conference NEUROTOXICOLOGY · March 1, 2003 Link to item Cite

Fetal chlorpyrifos exposure: Adverse effects on brain cell development and cholinergic biomarkers.

Conference TOXICOLOGICAL SCIENCES · March 1, 2003 Link to item Cite

Developmental neuro-and cardiotoxicity of terbutaline: DNA synthesis and neural biomarkers.

Conference TOXICOLOGICAL SCIENCES · March 1, 2003 Link to item Cite

Short-term nicotine exposure in adolescent rats elicits brain cell damage.

Conference TOXICOLOGICAL SCIENCES · March 1, 2003 Link to item Cite

Developmental neurotoxicity - The perspective from academia: Biological mechanisms versus regulatory issues

Conference NEUROTOXICOLOGY · March 1, 2003 Link to item Cite

Adrenergic receptor crosstalk during development: Adverse effect of tocolytics?

Conference TOXICOLOGICAL SCIENCES · March 1, 2003 Link to item Cite

Changes in serotonin receptors in brain regions of rats after neonatal exposure to chlorpyrifos.

Conference TOXICOLOGICAL SCIENCES · March 1, 2003 Link to item Cite

Developmental toxicity of terbutaline: critical periods for sex-selective effects on macromolecules and DNA synthesis in rat brain, heart, and liver.

Journal Article Brain Res Bull · January 15, 2003 beta-Adrenoceptors (betaARs) control cell replication/differentiation, and during development, signaling is not subject to desensitization. We examined the effects of terbutaline, a beta(2)AR agonist used as a tocolytic, on development in rat brain regions ... Full text Link to item Cite

Transcriptional biomarkers distinguish between vulnerable periods for developmental neurotoxicity of chlorpyrifos: Implications for toxicogenomics.

Journal Article Brain Res Bull · January 15, 2003 The widespread use of organophosphate insecticides has raised concern about neurotoxic effects of fetal and childhood exposures. Studies in rats show that chlorpyrifos (CPF) elicits CNS cell damage, in part, through noncholinergic mechanisms that involve a ... Full text Link to item Cite

Alterations in PKCgamma in the mouse hippocampus after prenatal exposure to heroin: a link from cell signaling to behavioral outcome.

Journal Article Brain Res Dev Brain Res · January 10, 2003 Administration of heroin to pregnant mice evokes neurochemical and behavioral deficits consequent to disruption of septohippocampal cholinergic innervation, notably involving desensitization of the ability of cholinergic receptors to activate PKC activity. ... Full text Link to item Cite

Effect of maternal smoking on fetal catecholamine concentrations at birth.

Journal Article Pediatr Res · January 2003 The aim of this study was to compare catecholamine concentrations in the fetal umbilical artery cord blood from the offspring of smokers versus the offspring of nonsmokers. Pregnant women who were self-identified as smokers (>/=10 cigarettes per day throug ... Full text Link to item Cite

Sea urchin embryos and larvae as biosensors for neurotoxicants.

Journal Article Curr Protoc Toxicol · 2003 Sea urchin embryos and larvae provide an inexpensive high-throughput system for determining developmental actions of neuropharmacologic agents or environmental neurotoxins in both applied and basic biologic contexts. The use of this system for the testing ... Full text Link to item Cite

Beta-adrenoceptor control of G protein function in the neonate: determinant of desensitization or sensitization.

Journal Article Am J Physiol Regul Integr Comp Physiol · November 2002 Neonatal beta-adrenoceptors (beta-ARs) are resistant to agonist-induced desensitization. We examined the functioning of G(i) and G(s) after repeated administration of beta-AR agonists to newborn rats. Isoproterenol (beta(1)/beta(2) agonist) obtunded G(i) f ... Full text Link to item Cite

Developmental neurotoxicity of chlorpyrifos: what is the vulnerable period?

Journal Article Environ Health Perspect · November 2002 Previously, we found that exposure of neonatal rats to chlorpyrifos (CPF) produced brain cell damage and loss, with resultant abnormalities of synaptic development. We used the same biomarkers to examine prenatal CPF treatment so as to define the critical ... Full text Link to item Cite

Adolescent nicotine administration alters serotonin receptors and cell signaling mediated through adenylyl cyclase.

Journal Article Brain Res · October 4, 2002 Nicotine is a neuroteratogen that targets synaptic function during critical developmental stages and recent studies indicate that CNS vulnerability extends into adolescence, the age at which smoking typically commences. We administered nicotine to adolesce ... Full text Link to item Cite

Are developing β-adrenoceptors able to desensitize? Acute and chronic effects of β-agonists in neonatal heart and liver

Journal Article American Journal of Physiology - Regulatory Integrative and Comparative Physiology · August 20, 2002 During fetal and neonatal development, β-adrenergic receptors (β-ARs) appear to be resistant to desensitization by β-agonist drugs. To determine the mechanisms underlying the regulatory differences between adults and neonates, we administered isoproterenol ... Cite

Are developing beta-adrenoceptors able to desensitize? Acute and chronic effects of beta-agonists in neonatal heart and liver.

Journal Article Am J Physiol Regul Integr Comp Physiol · July 2002 During fetal and neonatal development, beta-adrenergic receptors (beta-ARs) appear to be resistant to desensitization by beta-agonist drugs. To determine the mechanisms underlying the regulatory differences between adults and neonates, we administered isop ... Full text Link to item Cite

Cell signaling as a target and underlying mechanism for neurobehavioral teratogenesis.

Journal Article Ann N Y Acad Sci · June 2002 A wide variety of drugs and chemicals elicit neurobehavioral teratogenesis. Surprisingly, however, despite the obvious differences among unrelated compounds, the behavioral outcomes often display striking similarities, such as cognitive and attentional def ... Full text Link to item Cite

beta-Adrenergic modulation of muscarinic cholinergic receptor expression and function in developing heart.

Journal Article Am J Physiol Regul Integr Comp Physiol · May 2002 Imbalances of beta-adrenoceptor (beta-AR) and muscarinic ACh receptor (mAChR) input are thought to underlie perinatal cardiovascular abnormalities in conditions such as sudden infant death syndrome. Administration of isoproterenol, a beta(1)/beta(2)-AR ago ... Full text Link to item Cite

Developmental neurotoxicity of chlorpyrifos: Defining the vulnerable period

Journal Article FASEB JOURNAL · March 22, 2002 Link to item Cite

Terbutaline tocolysis: a source of developmental brain damage?

Journal Article FASEB JOURNAL · March 22, 2002 Link to item Cite

Heterologous sensitization and desensitization of beta-adrenoceptor/adenylyl cyclase signaling in neonatal rat heart

Journal Article FASEB JOURNAL · March 20, 2002 Link to item Cite

Chlorpyrifos targets developing glia: effects on glial fibrillary acidic protein.

Journal Article Brain Res Dev Brain Res · February 28, 2002 The organophosphate pesticide, chlorpyrifos (CPF), is a developmental neurotoxicant. In cell cultures, CPF affects gliotypic cells to a greater extent than neuronotypic cells, suggesting that glial development is a specific target. We administered CPF to d ... Full text Link to item Cite

Perinatal exposure to environmental tobacco smoke upregulates nicotinic cholinergic receptors in monkey brain.

Journal Article Brain Res Dev Brain Res · February 28, 2002 In humans, perinatal exposure to environmental tobacco smoke (ETS) is associated with neurobehavioral deficits. In the current study, we exposed Rhesus monkeys to ETS in late gestation and in the early neonatal period, and examined changes in neurotransmit ... Full text Link to item Cite

Nicotine and the adolescent brain: insights from an animal model.

Journal Article Neurotoxicol Teratol · 2002 Tobacco use in adolescence represents one of the major challenges to the future of public health. Whereas numerous studies have explored the consequences of fetal or adult nicotine effects, little or no basic research has been conducted for nicotine during ... Full text Link to item Cite

Prenatal nicotine exposure evokes alterations of cell structure in hippocampus and somatosensory cortex.

Journal Article J Pharmacol Exp Ther · January 2002 Offspring of women who smoke during pregnancy show behavioral abnormalities, including increased incidence of attentional deficit, learning disabilities, and cognitive dysfunction. Animal models indicate that nicotine elicits changes in neural cell replica ... Full text Link to item Cite

Prenatal chlorpyrifos exposure in rats causes persistent behavioral alterations.

Journal Article Neurotoxicol Teratol · 2002 Use of chlorpyrifos (CPF) has been curtailed due to its developmental neurotoxicity. In rats, postnatal CPF administration produces lasting changes in cognitive performance, but less information is available about the effects of prenatal exposure. We admin ... Full text Link to item Cite

Heroin neuroteratogenicity: targeting adenylyl cyclase as an underlying biochemical mechanism.

Journal Article Brain Res Dev Brain Res · December 14, 2001 Prenatal heroin exposure evokes neurochemical and behavioral deficits that in part, reflect disruption of septohippocampal cholinergic function. In earlier studies, we found that cholinergic synaptic defects involve changes in proteins, like protein kinase ... Full text Link to item Cite

Beta-adrenoceptor-mediated cell signaling in the neonatal heart and liver: responses to terbutaline.

Journal Article Am J Physiol Regul Integr Comp Physiol · December 2001 Terbutaline, a beta(2)-adrenoceptor (beta(2)-AR) agonist, is a widely used tocolytic that also crosses the placenta to stimulate fetal beta-ARs. The current study examines the effects of terbutaline administered to neonatal rats. Terbutaline (10 mg/kg sc) ... Full text Link to item Cite

Beta-adrenoceptor signaling in the developing brain: sensitization or desensitization in response to terbutaline.

Journal Article Brain Res Dev Brain Res · November 26, 2001 Beta(2)-adrenoceptor agonists are commonly used to arrest preterm labor but they also penetrate the placenta to stimulate fetal beta-adrenergic receptors (betaAR), and have been implicated in subsequent neurobehavioral deficits. We administered terbutaline ... Full text Link to item Cite

[Cholinergic regulation of the sea urchin embryonic and larval development].

Journal Article Ross Fiziol Zh Im I M Sechenova · November 2001 Choline esters of polyenoic fatty acids block cleavage divisions of sea urchins and evoke the formation of one-cell multinuclear embryos. If the fatty acids AA-Ch or DHA-Ch are added at the mid or late blastula stage, many cells are extruded, forming extra ... Link to item Cite

Neonatal chlorpyrifos administration elicits deficits in immune function in adulthood: a neural effect?

Journal Article Brain Res Dev Brain Res · October 24, 2001 Neural input plays a key role in the establishment of immune function, and environmental agents or drugs that interfere with the development of the nervous system elicit corresponding immunologic deficits. In the current study, we gave neonatal rats the wi ... Full text Link to item Cite

Adolescent nicotine: deficits in immune function.

Journal Article Brain Res Dev Brain Res · October 24, 2001 Maternal cigarette smoking during pregnancy is known to alter immune function in the offspring and recent studies with animals indicate that prenatal nicotine exposure leads to lasting deficiencies in T-lymphocyte mitogenic responses, likely through excess ... Full text Link to item Cite

Regulation of fetal cardiac and hepatic beta-adrenoceptors and adenylyl cyclase signaling: terbutaline effects.

Journal Article Am J Physiol Regul Integr Comp Physiol · October 2001 Terbutaline (Ter), a beta(2)-adrenergic agonist used in preterm labor, stimulates fetal beta-adrenoceptors (beta-ARs). We administered Ter to pregnant rats on gestational days 17-20 and examined beta-ARs and adenylyl cyclase (AC) signaling in heart and liv ... Full text Link to item Cite

Fetal and adolescent nicotine administration: effects on CNS serotonergic systems.

Journal Article Brain Res · September 28, 2001 Nicotine is a neuroteratogen that targets synaptic function during critical developmental stages and recent studies indicate that CNS vulnerability extends into adolescence, the time that smoking typically commences. We administered nicotine to pregnant or ... Full text Link to item Cite

Alterations in serotonin transporter expression in brain regions of rats exposed neonatally to chlorpyrifos.

Journal Article Brain Res Dev Brain Res · September 23, 2001 Chlorpyrifos (CPF), one of the most widely-used organophosphate pesticides, is a suspected neuroteratogen. We administered CPF to neonatal rats on postnatal days (PN) 1-4 (1 mg/kg) or PN11-14 (5 mg/kg), treatments devoid of overt toxicity. At the end of th ... Full text Link to item Cite

Persistent behavioral consequences of neonatal chlorpyrifos exposure in rats.

Journal Article Brain Res Dev Brain Res · September 23, 2001 Chlorpyrifos (CPF) is a widely used insecticides which has been shown to alter brain cell development. The current project was conducted to determine whether there are persistent behavioral effects of early [1 mg/kg/day postnatal days (PNDs) 1-4] or late ( ... Full text Link to item Cite

Developmental neurotoxicity of chlorpyrifos modeled in vitro: comparative effects of metabolites and other cholinesterase inhibitors on DNA synthesis in PC12 and C6 cells.

Journal Article Environ Health Perspect · September 2001 The widely used organophosphate pesticide chlorpyrifos is a suspected neuroteratogen. In the current study, we compared the effects of chlorpyrifos and its major metabolites in two in vitro models, neuronotypic PC12 cells and gliotypic C6 cells. Chlorpyrif ... Full text Link to item Cite

An invertebrate model of the developmental neurotoxicity of insecticides: effects of chlorpyrifos and dieldrin in sea urchin embryos and larvae.

Journal Article Environ Health Perspect · July 2001 Chlorpyrifos targets mammalian brain development through a combination of effects directed at cholinergic receptors and intracellular signaling cascades that are involved in cell differentiation. We used sea urchin embryos as an invertebrate model system t ... Full text Link to item Cite

Persistent cholinergic presynaptic deficits after neonatal chlorpyrifos exposure.

Journal Article Brain Res · June 1, 2001 The commonly-used organophosphate insecticide, chlorpyrifos (CPF), impairs brain cell development, axonogenesis and synaptogenesis. In the current study, we administered CPF to neonatal rats on postnatal (PN) days 1-4 (1 mg/kg) or PN11-14 (5 mg/kg), treatm ... Full text Link to item Cite

Perinatal exposure to environmental tobacco smoke induces adenylyl cyclase and alters receptor-mediated cell signaling in brain and heart of neonatal rats.

Journal Article Brain Res · April 13, 2001 Perinatal exposure to environmental tobacco smoke (ETS) has adverse effects on neurobehavioral development. In the current study, rats were exposed to ETS during gestation, during the early neonatal period, or both. Brains and hearts were examined for alte ... Full text Link to item Cite

Signalling crosstalk during development: Does early stimulation of beta-adrenergic receptors control the expression of muscarinic cholinergic receptors?

Journal Article FASEB JOURNAL · March 7, 2001 Link to item Cite

Are fetal or neonatal beta-adrenergic receptors capable of downregulation or desensitization?

Journal Article FASEB JOURNAL · March 7, 2001 Link to item Cite

Generation of reactive oxygen species by xanthine derivatives in MDA-MB-231 human breast cancer cells.

Journal Article Breast Cancer Res Treat · March 2001 Theophylline reduces cell number in MDA-MB-231 cells through mechanisms over and above phosphodiesterase inhibition. In the current study, we used an intracellular fluorescent dye to show that theophylline and, to a much greater extent, 3-isobutyl-1-methyl ... Full text Link to item Cite

Adolescent nicotine exposure produces immediate and long-term changes in CNS noradrenergic and dopaminergic function.

Journal Article Brain Res · February 23, 2001 Animal studies have only recently begun to address whether nicotine evokes unique or persistent effects on brain structure or function during adolescence, the period in which smokers typically begin their habit. In the current study, we examined the impact ... Full text Link to item Cite

Does the developmental neurotoxicity of chlorpyrifos involve glial targets? Macromolecule synthesis, adenylyl cyclase signaling, nuclear transcription factors, and formation of reactive oxygen in C6 glioma cells.

Journal Article Brain Res · February 9, 2001 The widespread use of chlorpyrifos (CPF) has raised major concerns about its potential to cause fetal or neonatal neurobehavioral damage, even at doses that do not evoke acute toxicity. CPF has been shown to inhibit replication of brain cells, to elicit al ... Full text Link to item Cite

Cholinergic regulation of the sea urchin embryonic and larval development

Journal Article Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova / Rossiiskaia akademiia nauk · January 1, 2001 Choline esters of polyenoic fatty acids block cleavage divisions of sea urchins and evoke the formation of one-cell multinuclear embryos. If the fatty acids AA-Ch or DHA-Ch are added at the mid or late blastula stage, many cells are extruded, forming extra ... Cite

Neural grafting reverses prenatal drug-induced alterations in hippocampal PKC and related behavioral deficits.

Journal Article Brain Res Dev Brain Res · December 29, 2000 Administration of heroin or phenobarbital to pregnant mice evokes neurochemical and behavioral deficits consequent to disruption of septohippocampal cholinergic innervation. The present study evaluates the relationship between the drug-induced biochemical ... Full text Link to item Cite

Neonatal polyamine depletion by alpha-difluoromethylornithine: effects on adenylyl cyclase cell signaling are separable from effects on brain region growth.

Journal Article Brain Res · December 22, 2000 Ornithine decarboxylase (ODC) and the polyamines play an essential role in brain cell replication and differentiation. We administered alpha-difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, to neonatal rats on postnatal days 5-12, during t ... Full text Link to item Cite

Antimitotic and cytotoxic effects of theophylline in MDA-MB-231 human breast cancer cells.

Journal Article Breast Cancer Res Treat · December 2000 A variety of cancer cell lines, including MDA-MB-231 human breast cancer cells, exhibit mitotic inhibition by cAMP. In earlier work, we found that the phosphodiesterase inhibitor, theophylline, reduced the number of cells and altered cellular morphology. I ... Full text Link to item Cite

Perinatal exposure to environmental tobacco smoke alters cell signaling in a primate model: autonomic receptors and the control of adenylyl cyclase activity in heart and lung.

Journal Article Brain Res Dev Brain Res · November 30, 2000 Perinatal exposure to environmental tobacco smoke (ETS) is known to have adverse effects on respiratory function in conjunction with changes in autonomic responses. In the current study, Rhesus monkeys were exposed to ETS during late gestation and in the e ... Full text Link to item Cite

Regional differences in brain monoamine oxidase subtypes in an animal model of geriatric depression: effects of olfactory bulbectomy in young versus aged rats.

Journal Article Brain Res · November 3, 2000 Geriatric depression is often associated dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis, and with poor responsiveness to antidepressants that work through inhibition of monoamine reuptake; accordingly, it has been suggested that MAO inhibit ... Full text Link to item Cite

Persistent and delayed behavioral changes after nicotine treatment in adolescent rats.

Journal Article Brain Res · October 13, 2000 Despite the increasing use of tobacco by adolescents, few animal studies have addressed the neurobehavioral consequences of nicotine exposure during this period. We administered nicotine to adolescent rats via continuous infusion on postnatal days (PN) 30 ... Full text Link to item Cite

Cellular determinants of reduced adaptability of the aging brain: neurotransmitter utilization and cell signaling responses after MDMA lesions.

Journal Article Brain Res · October 6, 2000 Senescence is accompanied by the loss of neurons and synapses, and the maintenance of function depends on adaptive change at the levels of synaptic activity and cellular responsiveness. In the current study, we administered the neurotoxin MDMA, to young an ... Full text Link to item Cite

Adolescent nicotine exposure alters cardiac autonomic responsiveness: beta-adrenergic and m2-muscarinic receptors and their linkage to adenylyl cyclase.

Journal Article Brain Res · September 29, 2000 Recent work indicates that adolescent smokers have an abnormally high incidence of heart rate irregularities. In the current study, adolescent rats received nicotine by continuous infusion from postnatal days (PN) 30-47.5, using a regimen designed to produ ... Full text Link to item Cite

Neurobehavioral damage to cholinergic systems caused by prenatal exposure to heroin or phenobarbital: cellular mechanisms and the reversal of deficits by neural grafts.

Journal Article Brain Res Dev Brain Res · August 30, 2000 Despite the basic differences in their underlying biological targets, prenatal exposure to heroin or phenobarbital produces similar syndromes of neurobehavioral deficits, involving defects in septohippocampal cholinergic innervation-related behaviors. At t ... Full text Link to item Cite

Modeling adolescent nicotine exposure: effects on cholinergic systems in rat brain regions.

Journal Article Brain Res · August 4, 2000 Smoking among teenagers is increasing and the initiation of tobacco use during adolescence is associated with subsequently higher cigarette consumption and lower rates of quitting. Few animal studies have addressed whether adolescent nicotine exposure exer ... Full text Link to item Cite

Chlorpyrifos exposure during a critical neonatal period elicits gender-selective deficits in the development of coordination skills and locomotor activity.

Journal Article Brain Res Dev Brain Res · June 30, 2000 The widespread use of chlorpyrifos has raised concern about the potential consequences of fetal and childhood exposure. Previous studies have shown that apparently subtoxic doses of chlorpyrifos are nevertheless capable of affecting brain development by in ... Full text Link to item Cite

Is oxidative stress involved in the developmental neurotoxicity of chlorpyrifos?

Journal Article Brain Res Dev Brain Res · June 30, 2000 The increasing use of chlorpyrifos (CPF) has elicited concern about neurotoxic effects on the fetus and neonate. CPF targets a number of events specific to brain development, over and above the ability of its active metabolite, CPF oxon, to inhibit choline ... Full text Link to item Cite

An animal model of adolescent nicotine exposure: effects on gene expression and macromolecular constituents in rat brain regions.

Journal Article Brain Res · June 9, 2000 Nearly all smokers begin tobacco use in adolescence, and approximately 25% of US teenagers are daily smokers. Prenatal nicotine exposure is known to produce brain damage, to alter synaptic function and to cause behavioral anomalies, but little or no work h ... Full text Link to item Cite

Neonatal chlorpyrifos exposure targets multiple proteins governing the hepatic adenylyl cyclase signaling cascade: implications for neurotoxicity.

Journal Article Brain Res Dev Brain Res · May 11, 2000 Chlorpyrifos has been hypothesized to interact with receptors and transduction proteins involved in the production of cyclic AMP, contributing to adverse effects on cell replication and differentiation. We studied the effects of neonatal chlorpyrifos expos ... Full text Link to item Cite

Ontogeny of G-protein expression: control by beta-adrenoceptors.

Journal Article Brain Res Dev Brain Res · April 14, 2000 Cardiac cell homeostasis is maintained in the face of excessive beta-adrenoceptor stimulation through the process of desensitization. Desensitization is not an inherent property of these cells but rather is acquired during development; neonates given beta- ... Full text Link to item Cite

Beta-adrenoceptor signaling and its control of cell replication in MDA-MB-231 human breast cancer cells.

Journal Article Breast Cancer Res Treat · March 2000 MDA-MB-231 human breast cancer cells express high beta-adrenoceptor levels, predominantly the beta2 subtype. Receptor stimulation by isoproterenol evoked immediate reductions in DNA synthesis which were blocked completely by propranolol and were of the sam ... Full text Link to item Cite

Developmental neurotoxicity of chlorpyrifos in vivo and in vitro: effects on nuclear transcription factors involved in cell replication and differentiation.

Journal Article Brain Res · February 28, 2000 Chlorpyrifos is a widely used organophosphate insecticide that is a suspected developmental neurotoxin. Although chlorpyrifos exerts some effects through cholinesterase inhibition, recent studies suggest additional, direct actions on developing cells. We a ... Full text Link to item Cite

The use of pharmacotherapies for smoking cessation during pregnancy.

Journal Article Tob Control · 2000 Full text Link to item Cite

Receptors for abused drugs: development and plasticity.

Journal Article Neurotoxicol Teratol · 2000 Full text Link to item Cite

Adolescent nicotine exposure causes persistent upregulation of nicotinic cholinergic receptors in rat brain regions.

Journal Article Brain Res · December 18, 1999 Whereas numerous studies have explored the consequences of fetal or adult nicotine exposure, little or no basic research has been conducted for nicotine exposure during adolescence, the developmental period in which regular cigarette use typically begins. ... Full text Link to item Cite

Chlorpyrifos releases norepinephrine from adult and neonatal rat brain synaptosomes.

Journal Article Brain Res Dev Brain Res · December 10, 1999 Exposure of developing animals to apparently subtoxic doses of chlorpyrifos (CPF) during a critical period of synaptogenesis has been shown to affect catecholaminergic synaptic development and neuronal activity separably from its inhibition of cholinestera ... Full text Link to item Cite

Agonist-induced sensitization of beta-adrenoceptor signaling in neonatal rat heart: expression and catalytic activity of adenylyl cyclase.

Journal Article J Pharmacol Exp Ther · November 1999 Agonist stimulation of neonatal cardiac beta-adrenoceptors produces heterologous sensitization of adenylyl cyclase (AC) signaling, rather than desensitization, as seen in adults. We examined the ontogenetic patterns of AC expression and activity, and evalu ... Link to item Cite

Response to the letter of Hanley et al. ([1999] Teratology 59:323-324), concerning the article by Roy et al. ([1998] Teratology 58:62-68).

Journal Article Teratology · October 1999 Full text Link to item Cite

Neonatal chlorpyrifos exposure alters synaptic development and neuronal activity in cholinergic and catecholaminergic pathways.

Journal Article Brain Res Dev Brain Res · August 5, 1999 After routine home application of chlorpyrifos (CPF), infant and child exposures can exceed acceptable levels. We treated neonatal rats daily on postnatal days (PN) 1-4 (1 mg/kg) or days 11-14 (5 mg/kg), treatments that evoked no overt signs of toxicity. E ... Full text Link to item Cite

Modeling geriatric depression in animals: biochemical and behavioral effects of olfactory bulbectomy in young versus aged rats.

Journal Article J Pharmacol Exp Ther · April 1999 Geriatric depression exhibits biological and therapeutic differences relative to early-onset depression. We studied olfactory bulbectomy (OBX), a paradigm that shares major features of human depression, in young versus aged rats to determine mechanisms und ... Link to item Cite

Modeling the developmental neurotoxicity of chlorpyrifos in vitro: macromolecule synthesis in PC12 cells.

Journal Article Toxicol Appl Pharmacol · April 1, 1999 Full text Link to item Cite

Cholinergic receptors in heart and brainstem of rats exposed to nicotine during development: implications for hypoxia tolerance and perinatal mortality.

Journal Article Brain Res Dev Brain Res · March 12, 1999 Cigarette smoking during pregnancy increases the incidence of perinatal mortality and Sudden Infant Death Syndrome (SIDS). We have evaluated prenatal or postnatal nicotine exposure in developing rats to examine the potential role of altered neurotransmitte ... Full text Link to item Cite

Prenatal nicotine exposure induces genes associated with apoptosis in the developing brain

Journal Article FASEB JOURNAL · March 12, 1999 Link to item Cite

Cellular mechanisms underlying agonist-induced heterologous sensitization of beta-adrenergic receptor signaling in neonatal rat heart

Journal Article FASEB JOURNAL · March 12, 1999 Link to item Cite

Ontogeny of cardiac beta-adrenoceptor desensitization mechanisms: agonist treatment enhances receptor/G-protein transduction rather than eliciting uncoupling.

Journal Article J Mol Cell Cardiol · February 1999 In the fetus and neonate, beta-adrenoceptor stimulation fails to produce physiological desensitization. The current study explores the mechanisms underlying the response pattern in neonatal rats. Homologous cardiac beta-adrenergic desensitization caused by ... Full text Link to item Cite

Developmental cholinotoxicants: nicotine and chlorpyrifos.

Journal Article Environ Health Perspect · February 1999 The stimulation of cholinergic receptors in target cells during a critical developmental period provides signals that influence cell replication and differentiation. Accordingly, environmental agents that promote cholinergic activity evoke neurodevelopment ... Full text Link to item Cite

Persistent c-fos induction by nicotine in developing rat brain regions: interaction with hypoxia.

Journal Article Pediatr Res · January 1999 Prenatal nicotine exposure evokes postnatal CNS cell loss. We administered nicotine to pregnant rats throughout gestation and neonatal brains were examined for expression of c-fos, a nuclear transcription factor involved in differentiation and cell death. ... Full text Link to item Cite

Mary Bernheim and the discovery of monoamine oxidase.

Journal Article Brain Res Bull · 1999 Full text Link to item Cite

Nicotine evokes cell death in embryonic rat brain during neurulation.

Journal Article J Pharmacol Exp Ther · December 1998 Maternal cigarette smoking during pregnancy represents the most prevalent exposure to a suspected neuroteratogen, nicotine. Although animal models have demonstrated brain cell loss and synaptic abnormalities after prenatal nicotine exposure, the multiple e ... Link to item Cite

Glucocorticoid administration alters nuclear transcription factors in fetal rat brain: implications for the use of antenatal steroids.

Journal Article Brain Res Dev Brain Res · November 1, 1998 A recent Consensus Conference endorsed antenatal steroid use in prematurity, but indicated the need for future work on molecular and cellular effects on the developing brain. In the current study, pregnant rats were given dexamethasone during late gestatio ... Full text Link to item Cite

Effects of aging and glucocorticoid treatment on monoamine oxidase subtypes in rat cerebral cortex: therapeutic implications.

Journal Article Brain Res Bull · November 1, 1998 Dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis is more common in elderly depression than in younger cohorts, resulting in elevated glucocorticoid levels. Effectiveness of antidepressant drugs is also impaired in these patients. We evaluated ... Full text Link to item Cite

Glucocorticoid-targeting of the adenylyl cyclase signaling pathway in the cerebellum of young vs. aged rats.

Journal Article Brain Res · August 3, 1998 Glucocorticoids exacerbate aging-induced cell death, but relatively little is known about other CNS effects in senescence. We examined noradrenergic/adenylyl cyclase signaling in the cerebellum, which is a brain region that is susceptible to deterioration ... Full text Link to item Cite

Chlorpyrifos elicits mitotic abnormalities and apoptosis in neuroepithelium of cultured rat embryos.

Journal Article Teratology · August 1998 Chlorpyrifos is used increasingly as a pesticide in place of more toxic alternatives such as parathion. Although chlorpyrifos is not a potent dysmorphogen, recent reports that fetal or infant exposures may exceed acceptable limits have raised concern about ... Full text Link to item Cite

Modeling the developmental neurotoxicity of chlorpyrifos in vitro: macromolecule synthesis in PC12 cells.

Journal Article Toxicol Appl Pharmacol · July 1998 Exposure to apparently subtoxic doses of chlorpyrifos during late stages of brain development affects cell acquisition through a mixture of cholinergic and noncholinergic mechanisms. In the current study, we modeled these effects in vitro using rat pheochr ... Full text Link to item Cite

Consensus on postnatal deficits: comparability of human and animal findings.

Journal Article Ann N Y Acad Sci · June 21, 1998 Link to item Cite

Developmental neurotoxicity of chlorpyrifos: delayed targeting of DNA synthesis after repeated administration.

Journal Article Brain Res Dev Brain Res · June 15, 1998 Despite the fact that they recover more rapidly from cholinesterase inhibition than do adults, developing animals are more sensitive to delayed neurotoxicity caused by chlorpyrifos exposure. Previous studies indicate that acute, high dose chlorpyrifos expo ... Full text Link to item Cite

Fetal nicotine or cocaine exposure: which one is worse?

Journal Article J Pharmacol Exp Ther · June 1998 Despite extensive adverse publicity, tobacco use continues in approximately 25% of all pregnancies in the United States, overshadowing illicit drugs of abuse, including cocaine. The societal cost of maternal smoking is seen most readily in underweight newb ... Link to item Cite

Early biochemical detection of delayed neurotoxicity resulting from developmental exposure to chloropyrifos.

Journal Article Brain Res Bull · 1998 Developing animals are more sensitive than adults to the delayed neurotoxicity caused by chlorpyrifos exposure. In developing rat brain, chlorpyrifos doses that cause no discernible systemic toxicity and only a minor degree of cholinesterase inhibition, ne ... Full text Link to item Cite

Unique mechanisms of β-adrenoceptor sensitization and desensitization during development

Journal Article FASEB Journal · 1998 Receptor desensitization is the major mode by which cells limit the degree and duration of agonist-induced stimulation. In the case of cardiac β-adrenoceptors, we have shown that this is not an inherent property of cells but rather is acquired as a distinc ... Cite

The impact of fetal nicotine exposure on nervous system development and its role in sudden infant death syndrome

Conference NICOTINE SAFETY AND TOXICITY · January 1, 1998 Link to item Cite

Convergent control of serotonin transporter expression by glucocorticoids and cocaine in fetal and neonatal rat brain.

Journal Article Brain Res Dev Brain Res · December 19, 1997 Serotonin plays a trophic role in brain cell differentiation. In this study, expression of the serotonin presynaptic transporter protein, which regulates the extracellular serotonin concentration, was measured with [3H]paroxetine in rats exposed to dexamet ... Full text Link to item Cite

A critical period for the role of thyroid hormone in development of renal alpha-adrenergic receptors.

Journal Article Pediatr Res · July 1997 Adrenergic input influences renal cell replication/differentiation and the development of excretory function. Kidney cells make adrenoceptors before the arrival of the majority of nerve terminals, and the current study examines whether thyroid hormone play ... Full text Link to item Cite

Cellular mechanisms for developmental toxicity of chlorpyrifos: targeting the adenylyl cyclase signaling cascade.

Journal Article Toxicol Appl Pharmacol · July 1997 Developmental neurotoxicity caused by chlorpyrifos exposure is generally thought to target cholinesterase but chlorpyrifos may also act on cellular intermediates, such as adenylyl cyclase, that serve global functions in the coordination of cell development ... Full text Link to item Cite

Expression of mRNAs coding for the transforming growth factor-beta receptors in brain regions of euthyroid and hypothyroid neonatal rats and in adult brain.

Journal Article Brain Res Dev Brain Res · March 17, 1997 The TGF-beta family of peptides has been postulated to play a role in control of the cell cycle but also may act in the developing brain to influence neuronal differentiation and survival. Because reception of TGF-beta signals requires the simultaneous exp ... Full text Link to item Cite

Cryptic brain cell injury caused by fetal nicotine exposure is associated with persistent elevations of c-fos protooncogene expression.

Journal Article Brain Res · March 7, 1997 Neurobehavioral teratogenesis caused by prenatal nicotine exposure is associated with deficiencies in brain cell numbers that reflect, in part, effects on cell replication but that also involve delayed cell loss. In the current study, pregnant rats were gi ... Full text Link to item Cite

Neuronal control of cardiac and hepatic macromolecule synthesis in the neonatal rat: effects of sympathectomy.

Journal Article Pediatr Res · March 1997 Neurotransmitters are thought to influence cell development in their target tissues. In the current study, neonatal rats were given 6-hydroxydopamine to produce permanent sympathetic denervation, and the effects on cardiac and hepatic DNA and protein synth ... Full text Link to item Cite

Impaired cardiac function during postnatal hypoxia in rats exposed to nicotine prenatally: implications for perinatal morbidity and mortality, and for sudden infant death syndrome.

Journal Article Teratology · March 1997 Maternal smoking correlates highly with parturitional/neonatal death including SIDS; nicotine exposure of fetal rats reproduces the increased mortality when animals are tested postnatally with hypoxia. In the current study, pregnant rats received nicotine ... Full text Link to item Cite

Ontogeny of regulatory mechanisms for beta-adrenoceptor control of rat cardiac adenylyl cyclase: targeting of G-proteins and the cyclase catalytic subunit.

Journal Article J Mol Cell Cardiol · February 1997 Fetal and neonatal tissues are resistant to catecholamine-induced desensitization of essential physiological responses. We examined the mechanisms underlying the ontogeny of desensitization in neonatal rat heart for the beta-adrenergic receptor/adenylyl cy ... Full text Link to item Cite

Serotonin transporter expression in rat brain regions and blood platelets: aging and glucocorticoid effects.

Journal Article Biol Psychiatry · January 15, 1997 Hyperactivity of the hypothalamus-pituitary-adrenal axis is more common in elderly depression than in younger cohorts and glucocorticoids are known to influence serotonergic systems. The current study explores the interaction of glucocorticoids with aging ... Full text Link to item Cite

Chlorpyrifos interferes with cell development in rat brain regions.

Journal Article Brain Res Bull · 1997 Chlorpyrifos, one of the most widely used pesticides, exhibits greater toxicity during development than in adulthood. We administered chlorpyrifos to neonatal rats in doses spanning the threshold for systemic toxicity and examined developing brain regions ... Full text Link to item Cite

Dexamethasone suppression test identifies a subset of elderly depressed patients with reduced platelet serotonin transport and resistance to imipramine inhibition of transport.

Journal Article Depress Anxiety · 1997 Dysregulation of the hypothalamus-pituitary-adrenal axis (HPA) is more common in elderly patients with depression than in younger depressed patients, and glucocorticoids are known to influence serotonergic function. Elderly depressed patients are also repo ... Full text Link to item Cite

Ontogeny of beta-adrenoceptor/adenylyl cyclase desensitization mechanisms: the role of neonatal innervation.

Journal Article Brain Res · December 2, 1996 The ability of adrenergic stimulation to elicit desensitization of the beta-receptor/adenylyl cyclase signaling cascade is not an inherent property of cells but rather is acquired during the period in which sympathetic innervation develops. This study exam ... Full text Link to item Cite

Aging and glucocorticoids: effects on cell signaling mediated through adenylyl cyclase.

Journal Article J Pharmacol Exp Ther · November 1996 Abnormalities of hypothalamus-pituitary-adrenal axis regulation are common in the elderly and excess glucocorticoids have been implicated in the loss of neural function in aging. In the current study, we examined cell signaling mediated through adenylyl cy ... Link to item Cite

Do glucocorticoids contribute to the abnormalities in serotonin transporter expression and function seen in depression? An animal model.

Journal Article Biol Psychiatry · October 1, 1996 Adrenocorticosteroids and serotonergic neurons exert reciprocal regulatory actions, and both are abnormal in depression. We evaluated whether glucocorticoids influence the serotonin transporter in rat platelets and brain by infusing dexamethasone for 26 da ... Full text Link to item Cite

Programming of brainstem serotonin transporter development by prenatal glucocorticoids.

Journal Article Brain Res Dev Brain Res · May 31, 1996 Prenatal stress or exposure to excess glucocorticoids are known to alter central nervous system function and to result in lasting changes in reactions to stress. The potential involvement of specific elements of brainstem serotonergic neurons was examined ... Full text Link to item Cite

Expression of mRNA coding for the serotonin transporter in aged vs. young rat brain: differential effects of glucocorticoids.

Journal Article Brain Res · May 6, 1996 Serotonin transporter mRNA expression in midbrain of young and aged rats was measured after long-term infusion of dexamethasone (0.01 and 0.05 mg/kg/day). Aging alone had no effect. Dexamethasone significantly decreased expression in both young and old rat ... Full text Link to item Cite

Cardiac alpha-adrenergic receptor expression is regulated by thyroid hormone during a critical developmental period.

Journal Article J Mol Cell Cardiol · May 1996 Although thyroid hormone is obligatory for the development of cardiac beta-adrenergic receptors, it is difficult to assign a specific role for the hormone in receptor ontogeny because beta-receptor expression is affected similarly in the adult. We have det ... Full text Link to item Cite

Atypical regulation of hepatic adenylyl cyclase and adrenergic receptors during a critical developmental period: agonists evoke supersensitivity accompanied by failure of receptor down-regulation.

Journal Article Pediatr Res · April 1996 Ordinarily, beta-adrenergic receptors and responses linked to the receptors increase with development but in the liver, beta-receptors are higher in the fetus and neonate than in adulthood. We examined how hepatic beta-receptor signaling mediated through a ... Full text Link to item Cite

High affinity choline transporter status in Alzheimer's disease tissue from rapid autopsy.

Journal Article Ann N Y Acad Sci · January 17, 1996 The degeneration of nucleus basalis cholinergic neurons in Alzheimers disease (AD) has led to therapies that attempt to increase the synaptic availability of acetylcholine in the remaining cholinergic nerve terminals and to thereby reverse or slow the prog ... Full text Link to item Cite

Can intracellular signalling pathways predict developmental abnormalities?

Journal Article Biomarkers · 1996 Abstract Sensitivity of the adenylyl cyclase/c-fos protooncogene cascade to β-adrenergic agonists and glucocorticoids in foetal rat We examined whether measurements of adenylyl cyclase and its control of c-fos protooncogene mRNA expression in mid-gestation ... Full text Link to item Cite

Does concurrent or prior nicotine exposure interact with neonatal hypoxia to produce cardiac cell damage?

Journal Article Teratology · November 1995 Cigarette smoking during pregnancy exposes the fetus to both nicotine and hypoxia/ischemia; postnatal exposure to second-hand smoke also involves substances that cause hypoxia (CO, HCN). Although developing cardiac cells are more resistant to hypoxia-induc ... Full text Link to item Cite

Beta-adrenoceptor control of cardiac adenylyl cyclase during development: agonist pretreatment in the neonate uniquely causes heterologous sensitization, not desensitization.

Journal Article Brain Res · October 2, 1995 In the adult, increased stimulation of postsynaptic receptor sites produces compensatory desensitization that reduces tissue responsiveness. During development, however, responses in most systems increase with age and with the maturation of neuronal inputs ... Full text Link to item Cite

Developmental neurotoxicity of chlorpyrifos: cellular mechanisms.

Journal Article Toxicol Appl Pharmacol · September 1995 Chlorpyrifos, one of the most widely used pesticides, exhibits greater toxicity during development than in adulthood. We administered chlorpyrifos to neonatal rats in apparently subtoxic doses that caused no mortality and little or no weight deficits and e ... Full text Link to item Cite

Neural input and the development of adrenergic intracellular signaling: neonatal denervation evokes neither receptor upregulation nor persistent supersensitivity of adenylate cyclase.

Journal Article Brain Res Dev Brain Res · August 28, 1995 In the adult, denervation of adrenergic target tissues leads to compensatory upregulation of receptor sites and to supersensitive responses. When 6-hydroxydopamine (6-OHDA) was given to neonatal rats, cardiac beta-receptors failed to show significant upreg ... Full text Link to item Cite

Beta-adrenergic control of c-fos expression in fetal and neonatal rat tissues: relationship to cell differentiation and teratogenesis.

Journal Article Toxicol Appl Pharmacol · August 1995 beta-Adrenergic receptors appear in noradrenergic target tissues well before the arrival of nerve terminals, and are thought to play a role in the control of cell differentiation. We examined the ability of beta-agonists to stimulate expression of the nucl ... Full text Link to item Cite

Role of presynaptic input in the ontogeny of adrenergic cell signaling in rat brain: beta receptors, adenylate cyclase and c-fos protooncogene expression.

Journal Article J Pharmacol Exp Ther · April 1995 Neurotransmitters act as trophic factors during brain development, regulating expression of genes that control cellular differentiation. One example of this trophism is the beta adrenergic signaling cascade: activation of beta receptors leads sequentially ... Link to item Cite

Cocaine inhibits central noradrenergic and dopaminergic activity during the critical developmental period in which catecholamines influence cell development.

Journal Article Brain Res Dev Brain Res · March 16, 1995 Cocaine produces neurobehavioral damage in the fetus and neonate both through its ischemic actions and through direct effects mediated by the drug within the developing brain. The replication and differentiation of catecholaminergic target cells are contro ... Full text Link to item Cite

Effect of corticosteroids for fetal maturation on perinatal outcomes. NIH Consensus Development Panel on the Effect of Corticosteroids for Fetal Maturation on Perinatal Outcomes.

Journal Article JAMA · February 1, 1995 OBJECTIVE: To develop a consensus on the use of antenatal corticosteroids for fetal maturation in preterm infants. PARTICIPANTS: A nonfederal, nonadvocate, 16-member consensus panel including representatives from neonatology, obstetrics, family medicine, b ... Full text Link to item Cite

The developmental switch in ventricular myosin expression in vivo is not triggered by an increase in cyclic AMP.

Journal Article Reprod Fertil Dev · 1995 Ventricular myosin heavy chain (HC) expression undergoes a rapid change from the beta to the alpha isoform shortly after birth. Thyroid hormone is required for this transition to occur, but the time course of developmental changes in circulating thyroid ho ... Full text Link to item Cite

Modulation of hepatic adrenergic receptor ontogeny by thyroid hormone.

Journal Article Res Commun Mol Pathol Pharmacol · January 1995 During hepatic development, beta-adrenergic receptors are replaced by alpha 1-receptors, an important event in the switchover from neonatal to adult glucose metabolism. In mature tissues, expression of adrenergic receptor subtypes is regulated, in part, by ... Link to item Cite

Loss of neonatal hypoxia tolerance after prenatal nicotine exposure: implications for sudden infant death syndrome.

Journal Article Brain Res Bull · 1995 Maternal cigarette smoking has a high correlation with sudden Infant Death Syndrome, a condition in which cardiorespiratory failure occurs during an hypoxic episode, as in sleep apnea. Pregnant rats were given nicotine infusions of 2 or 6 mg/kg/day through ... Full text Link to item Cite

DEVELOPMENTAL EFFECTS OF NICOTINE

Conference EFFECTS OF NICOTINE ON BIOLOGICAL SYSTEMS II · January 1, 1995 Link to item Cite

Beta-adrenergic receptor overexpression in the fetal rat: distribution, receptor subtypes, and coupling to adenylate cyclase activity via G-proteins.

Journal Article Toxicol Appl Pharmacol · December 1994 Biogenic amines are hypothesized to play a role in the control of cell differentiation. We assessed the development of beta-adrenergic receptors and their linkage to adenylate cyclase activity in order to determine whether catecholaminergic cell signaling ... Full text Link to item Cite

In search of a mechanism for receptor-mediated neurobehavioral teratogenesis by nicotine: catecholamine release by nicotine in immature rat brain regions.

Journal Article Brain Res Dev Brain Res · October 14, 1994 Nicotine disrupts central nervous system development through interactions with nicotinic cholinergic receptors found in immature brain, leading to discoordination of target cell replication and differentiation. However, it is unclear whether the net result ... Full text Link to item Cite

Role of thyroid status in the ontogeny of adrenergic cell signaling in rat brain: beta receptors, adenylate cyclase, ornithine decarboxylase and c-fos protooncogene expression.

Journal Article J Pharmacol Exp Ther · October 1994 In adulthood, thyroid hormone regulates beta adrenergic responsiveness. We addressed whether similar processes operate in the developing brain, thus playing a role in neurotransmitter control of target cell differentiation. Rats were made hyperthyroid [tri ... Link to item Cite

Overexpression of the high affinity choline transporter in cortical regions affected by Alzheimer's disease. Evidence from rapid autopsy studies.

Journal Article J Clin Invest · August 1994 Cholinergic deficits in Alzheimer's disease are typically assessed by choline acetyltransferase, the enzyme that synthesizes acetylcholine. However, the determining step in acetylcholine formation is choline uptake via a high affinity transporter in nerve ... Full text Link to item Cite

Glucocorticoids enhance intracellular signaling via adenylate cyclase at three distinct loci in the fetus: a mechanism for heterologous teratogenic sensitization?

Journal Article Toxicol Appl Pharmacol · July 1994 Although high doses of glucocorticoids are teratogenic, endogenous hormones are necessary for development. Because of the central role of cAMP to control cell differentiation, we examined the dose dependence, tissue selectivity, and critical periods involv ... Full text Link to item Cite

beta Adrenergic control of c-fos protooncogene expression in developing rat brain regions.

Journal Article J Pharmacol Exp Ther · June 1994 The protooncogene c-fos encodes a nuclear protein that acts as a powerful enhancer of gene transcription, and shares the same general patterns of reactivity to stimulation as ornithine decarboxylase, an essential enzyme in cell replication and differentiat ... Link to item Cite

Prenatal dexamethasone exposure causes loss of neonatal hypoxia tolerance: cellular mechanisms.

Journal Article Pediatr Res · May 1994 Glucocorticoids promote lung cell differentiation and thus enhance surfactant synthesis in the management of neonatal respiratory distress syndrome. Because they also accelerate differentiation in other targets, glucocorticoids may compromise physiologic r ... Link to item Cite

Cocaine exacerbates hypoxia-induced cell damage in the developing brain: effects on ornithine decarboxylase activity and protein synthesis.

Journal Article Biol Neonate · 1994 The immature brain is resistant to cell damage from hypoxia, such as that experienced during parturition. Because cocaine causes cerebral ischemia, we examined whether cocaine interferes with this resistance. On postnatal days 1, 4 or 8, neonatal rats were ... Full text Link to item Cite

Dexamethasone treatment in utero enhances neonatal cholinergic nerve terminal development in rat brain.

Journal Article Res Commun Chem Pathol Pharmacol · August 1993 Fetal glucocorticoid administration has been proposed to elicit both promotional and inhibitory effects on neuronal development. In the current study, pregnant rats were given 0.05, 0.2 or 0.8 mg/kg of dexamethasone on gestational days 17, 18 and 19, and t ... Link to item Cite

Effects of fetal dexamethasone exposure on postnatal control of cardiac adenylate cyclase: beta-adrenergic receptor coupling to Gs regulatory protein.

Journal Article Teratology · August 1993 In the adult, glucocorticoids have been shown to upregulate beta-adrenergic control of adenylate cyclase by a variety of mechanisms; glucocorticoids are also thought to play a role in development of cardiac adrenergic function. In the current study, pregna ... Full text Link to item Cite

Immediate decline in DNA synthesis in neonatal rat lung caused by exposure to 100% oxygen.

Journal Article Res Commun Chem Pathol Pharmacol · June 1993 Oxygen therapy in preterm infants is associated with bronchopulmonary dysplasia, but the relative importance of oxygen toxicity as compared to adverse effects of intubation and mechanical ventilation, remains uncertain. In freely-breathing neonatal rats, e ... Link to item Cite

FETAL DEXAMETHASONE EXPOSURE INCREASES VULNERABILITY TO HYPOXIA - CARDIAC CELLULAR MECHANISMS AND MORTALITY

Journal Article FASEB JOURNAL · February 23, 1993 Link to item Cite

ACUTE COCAINE EXPOSURE SENSITIZES NEONATAL RAT-BRAIN TO HYPOXIA

Journal Article FASEB JOURNAL · February 19, 1993 Link to item Cite

Fetal dexamethasone exposure interferes with establishment of cardiac noradrenergic innervation and sympathetic activity.

Journal Article Teratology · February 1993 Endogenous glucocorticoids provide natural differentiation signals for adrenergic neurons, and exposure to high exogenous steroid levels thus disrupts the timing of neuronal maturation. In the current study, pregnant rats were given 0.05, 0.2, or 0.8 mg/kg ... Full text Link to item Cite

Septohippocampal cholinergic changes after destruction of the A10-septal dopaminergic pathways.

Journal Article Neuropharmacology · February 1993 Mice were injected bilaterally into the septum with 6-hydroxydopamine and 6 weeks later the hippocampi were assayed for activity of choline acetyltransferase, muscarinic receptor binding capabilities and for formation of inositol phosphate in response to d ... Full text Link to item Cite

Differential development of cholinergic nerve terminal markers in rat brain regions: implications for nerve terminal density, impulse activity and specific gene expression.

Journal Article Brain Res · January 22, 1993 During critical developmental periods, cholinergic activity plays a key role in programming the development of target cells. In the current study, ontogeny of cholinergic terminals and their activity were contrasted in 4 brain regions of the fetal and neon ... Full text Link to item Cite

Prenatal cocaine and cell development in rat brain regions: effects on ornithine decarboxylase and macromolecules.

Journal Article Brain Res Bull · 1993 Prenatal cocaine exposure has been shown to cause neurobehavioral abnormalities. To determine whether effects on basic patterns of cell development underlie these functional deficits, we examined the aftermath of acute and chronic cocaine exposure on ontog ... Full text Link to item Cite

Acute effects of cocaine on ornithine decarboxylase activity in fetal and neonatal rat heart: evidence for cardiotoxicity.

Journal Article Biol Neonate · 1993 Fetal exposure to cocaine is associated with increased perinatal cardiac risk. In the current study, we examined the effects of acute cocaine administration on ornithine decarboxylase (ODC) activity in fetal and neonatal rat heart. ODC is a key regulatory ... Full text Link to item Cite

Glucocorticoids regulate the development of intracellular signaling: enhanced forebrain adenylate cyclase catalytic subunit activity after fetal dexamethasone exposure.

Journal Article Brain Res Bull · 1993 Although glucocorticoids cause growth retardation and interfere with cell development, selective promotion of some aspects of cell function also has been reported. The current study examines whether glucocorticoids enhance intracellular transduction mechan ... Full text Link to item Cite

Fetal nicotine exposure alters ontogeny of M1-receptors and their link to G-proteins.

Journal Article Neurotoxicol Teratol · 1993 Prenatal nicotine exposure has been shown to disrupt the development of cholinergic presynaptic tone and behaviors mediated through muscarinic cholinergic receptors. The current study examines nicotine's effects on ontogeny of postsynaptic muscarinic M1-re ... Full text Link to item Cite

Impact of fetal nicotine exposure on development of rat brain regions: critical sensitive periods or effects of withdrawal?

Journal Article Brain Res Bull · 1993 Fetal nicotine exposure evokes alterations in central nervous system structural, neurochemical, and behavioral development. In the current study, the relative importance of critical developmental exposure periods and withdrawal were examined by infusing ni ... Full text Link to item Cite

Fetal cocaine exposure causes persistent noradrenergic hyperactivity in rat brain regions: effects on neurotransmitter turnover and receptors.

Journal Article J Pharmacol Exp Ther · November 1992 Fetal cocaine exposure has been shown to cause neurobehavioral abnormalities related to ontogeny of catecholaminergic systems. In the current study, pregnant rats received cocaine (30 mg/kg s.c. daily) from gestational days 8 through 20 and markers of pres ... Link to item Cite

Fetal nicotine exposure ablates the ability of postnatal nicotine challenge to release norepinephrine from rat brain regions.

Journal Article Brain Res Dev Brain Res · October 23, 1992 Exposure of the fetus to nicotine is known to affect the function of noradrenergic pathways in the central nervous system. In the current study, synaptic mechanisms underlying the functional defects were evaluated in the offspring of pregnant rats given ni ... Full text Link to item Cite

Pituitary-thyroid axis reactivity to hyper- and hypothyroidism in the perinatal period: ontogeny of regulation of regulation and long-term programming of responses.

Journal Article J Dev Physiol · September 1992 To evaluate the role of perinatal thyroid status in the development of pituitary-thyroid axis regulation, we administered triiodothyronine to newborn rats for the first five days postpartum to achieve hyperthyroidism, or propylthiouracil perinatally to rat ... Link to item Cite

Altered development of basal and forskolin-stimulated adenylate cyclase activity in brain regions of rats exposed to nicotine prenatally.

Journal Article Brain Res Dev Brain Res · August 21, 1992 Exposure of the fetus to nicotine is known to affect cellular development, synaptogenesis and synaptic activity of a wide variety of neurotransmitter pathways in the central nervous system. In the current study, pregnant rats received nicotine infusions of ... Full text Link to item Cite

Fetal dexamethasone exposure alters macromolecular characteristics of rat brain development: a critical period for regionally selective alterations?

Journal Article Teratology · July 1992 Fetal glucocorticoid exposure retards postnatal growth and evokes abnormalities of nervous system structure and function. To examine the underlying mechanisms, we administered 0.2 or 0.8 mg/kg of dexamethasone to pregnant rats on gestational days 17, 18, a ... Full text Link to item Cite

Glucocorticoids accelerate the ontogenetic transition of cardiac ventricular myosin heavy-chain isoform expression in the rat: promotion by prenatal exposure to a low dose of dexamethasone.

Journal Article J Dev Physiol · July 1992 Cardiac myosin heavy chain expression undergoes a perinatal transition from predominance of beta-MHC to alpha-MHC. In the current study, we tested the effects of glucocorticoids in this early transition period, by treating pregnant rats with dexamethasone ... Link to item Cite

Thyroid hormone regulates ontogeny of beta adrenergic receptors and adenylate cyclase in rat heart and kidney: effects of propylthiouracil-induced perinatal hypothyroidism.

Journal Article J Pharmacol Exp Ther · June 1992 In mature animals, thyroid hormone is permissive for beta adrenergic receptor expression and adrenergic control of adenylate cyclase. To determine if endogenous thyroid hormones play a similar role in the development of receptors and transduction mechanism ... Link to item Cite

Transient postnatal elevation of norepinephrine content and turnover in brain regions of rats exposed to terbutaline prenatally: evidence for autoregulation of noradrenergic development?

Journal Article Res Commun Chem Pathol Pharmacol · June 1992 Terbutaline, a beta-adrenergic agonist used to arrest premature labor, crosses the placenta to affect fetal nervous system development. In the current study, pregnant rats were given 10 mg/kg of terbutaline on gestational days 17, 18 and 19 and the develop ... Link to item Cite

Promotional role for glucocorticoids in the development of intracellular signalling: enhanced cardiac and renal adenylate cyclase reactivity to beta-adrenergic and non-adrenergic stimuli after low-dose fetal dexamethasone exposure.

Journal Article J Dev Physiol · June 1992 Fetal exposure to high doses of glucocorticoids, as used to aid lung maturation in the therapy of Respiratory Distress Syndrome, causes growth retardation and interference with development of beta-adrenergic receptor-mediated cell signalling. The current s ... Link to item Cite

Overexpression of alpha 2-adrenergic receptors in fetal rat heart: receptors in search of a function.

Journal Article J Dev Physiol · April 1992 alpha 2-Adrenergic receptors are transiently overexpressed by many types of developing cells. In the current study, the developmental profile and cellular function of these receptors were examined in the fetal and neonatal rat heart. alpha 2-Receptors, ass ... Link to item Cite

Ontogenetic transition of cardiac myosin heavy chain isoforms in rat ventricle: effects of fetal exposure to beta-adrenergic agonists or antagonists.

Journal Article J Dev Physiol · April 1992 Cardiac myosin heavy chain (MHC) expression undergoes an ontogenetic transition from beta to alpha MHC isoforms. Although thyroid hormone plays a role in this change, the timing of the events suggests the participation of other factors. Using a new, denatu ... Link to item Cite

Thyroid hormone differentially regulates cellular development in neonatal rat heart and kidney.

Journal Article Teratology · March 1992 The role of thyroid hormone in the control of cardiac and renal cell development was examined in neonatal rats made hyperthyroid by administration of triiodothyronine (T3, 0.1 mg/kg s.c. on postnatal days 1-5) or hypothyroid by administration of propylthio ... Full text Link to item Cite

DO GLUCOCORTICOIDS PROMOTE THE DEVELOPMENTAL SHIFT OF CARDIAC MYOSIN HEAVY-CHAIN (MHC) EXPRESSION

Journal Article FASEB JOURNAL · February 26, 1992 Link to item Cite

Fetal dexamethasone exposure accelerates development of renal function: relationship to dose, cell differentiation and growth inhibition.

Journal Article J Dev Physiol · February 1992 Fetal exposure to high doses of glucocorticoids slows cellular development and impairs organ performance, in association with growth retardation. Nevertheless, low doses of glucocorticoids may enhance cell differentiation and accelerate specific functions. ... Link to item Cite

Deficits in development of central cholinergic pathways caused by fetal nicotine exposure: differential effects on choline acetyltransferase activity and [3H]hemicholinium-3 binding.

Journal Article Neurotoxicol Teratol · 1992 Nicotine has been hypothesized to induce neurobehavioral teratology by mimicking prematurely the natural developmental signals ordinarily communicated by the ontogeny of cholinergic synaptic transmission. In the current study, the effects of fetal nicotine ... Full text Link to item Cite

Glucocorticoids and the development of neuronal function: effects of prenatal dexamethasone exposure on central noradrenergic activity.

Journal Article Biol Neonate · 1992 Although glucocorticoids slow the development of most cell types, they have been hypothesized to promote the differentiation of catecholaminergic cells. In the current study, pregnant rats were given dexamethasone on gestational days 17, 18 and 19, and the ... Full text Link to item Cite

Effects of prenatal cocaine exposure on development of rat cardiac adrenergic receptors and their control of adenylate cyclase activity

Journal Article Research Communications in Substances of Abuse · January 1, 1992 Fetal exposure to cocaine is associated with increased perinatal cardiac risk. Because cocaine promotes adrenergic actions, we assessed the effects of cocaine on development of cardiac adrenergic receptors and cell signaling in the rat. Pregnant rats were ... Cite

Fetal dexamethasone exposure sensitizes neonatal rat brain to hypoxia: effects on protein and DNA synthesis.

Journal Article Brain Res Dev Brain Res · December 17, 1991 Fetal exposure to glucocorticoids is known to produce long-term alterations in cell development within the central nervous system. The current study examines whether some of the adverse effects of prenatal dexamethasone treatment on brain development repre ... Full text Link to item Cite

Ischemia contributes to adverse effects of cocaine on brain development: suppression of ornithine decarboxylase activity in neonatal rat.

Journal Article Brain Res Bull · December 1991 Exposure to cocaine during development has been shown to cause structural and functional alterations in the nervous system. In the current study, the mechanisms underlying these effects were examined in neonatal rats through measurement of ornithine decarb ... Full text Link to item Cite

Promotional role for glucocorticoids in the development of intracellular signalling: enhanced cardiac and renal adenylate cyclase reactivity to beta-adrenergic and non-adrenergic stimuli after low-dose fetal dexamethasone exposure.

Journal Article J Dev Physiol · December 1991 Fetal exposure to high doses of glucocorticoids, as used to aid lung maturation in the therapy of Respiratory Distress Syndrome, causes growth retardation and interference with development of beta-adrenergic receptor-mediated cell signalling. The current s ... Link to item Cite

Developmental shift from local to central control of norepinephrine release in the cardiac-sympathetic axis: effects of cocaine and related drugs.

Journal Article J Pharmacol Exp Ther · December 1991 Developmental exposure to cocaine is associated with cardiovascular abnormalities as well as neurobehavioral disturbances. Because of the profound influence of cocaine on noradrenergic neurotransmission, we examined its acute effects on norepinephrine rele ... Link to item Cite

Acute stimulation of ornithine decarboxylase in neonatal rat brain regions by nicotine: a central receptor-mediated process?

Journal Article Brain Res Dev Brain Res · November 19, 1991 Nicotine exposure during development alters central nervous system structure and function. In the current study, we examined the acute effects of nicotine (3 mg/kg) on developing rat brain by monitoring ornithine decarboxylase (ODC), a marker for perturbed ... Full text Link to item Cite

Thyroid hormone differentially regulates development of beta-adrenergic receptors, adenylate cyclase and ornithine decarboxylase in rat heart and kidney.

Journal Article J Dev Physiol · October 1991 In mature animals, thyroid hormone produces parallel up-regulation of beta-adrenergic receptor binding sites and their linkage to adenylate cyclase; during development, these same processes may be critical in establishing the set-point for subsequent adren ... Link to item Cite

Dose-dependent glucocorticoid effects on noradrenergic synaptogenesis in rat brain: ontogeny of [3H]desmethylimipramine binding sites after fetal exposure to dexamethasone.

Journal Article Res Commun Chem Pathol Pharmacol · July 1991 Glucocorticoid administration slows the development of many types of cells, but may selectively accelerate differentiation of catecholaminergic cells. In the current study, pregnant rats were given dexamethasone on gestational days 17, 18 and 19 and noradr ... Link to item Cite

Species differences in alpha 2-adrenergic regulation of platelet adenylate cyclase.

Journal Article Res Commun Chem Pathol Pharmacol · June 1991 Species differences in the ability of alpha 2-adrenergic receptors to down-regulate platelet adenylate cyclase activity were compared in platelet membranes derived from man, rabbit and rat. In all three, prostaglandin E1 and forskolin caused massive stimul ... Link to item Cite

Presynaptic input regulates development of beta-adrenergic control of rat brain ornithine decarboxylase: effects of 6-hydroxydopamine or propranolol.

Journal Article Brain Res Bull · June 1991 beta-Adrenergic control of ornithine decarboxylase (ODC) activity is exerted only during a critical period in central nervous system development, playing an important role in neurotransmitter modulation of cell replication and differentiation. The current ... Full text Link to item Cite

Neural factors in the development of renal function: effect of neonatal central catecholaminergic lesions with 6-hydroxydopamine.

Journal Article J Dev Physiol · June 1991 Peripheral sympathetic neurons are thought to provide trophic regulatory signals for development of their target tissues. In the current study, we investigated the role of sympathetic tone in the functional development of the kidney in rats, using neonatal ... Link to item Cite

Fetal dexamethasone exposure impairs cellular development in neonatal rat heart and kidney: effects on DNA and protein in whole tissues.

Journal Article Teratology · April 1991 Fetal glucocorticoid exposure causes postnatal growth retardation. To examine the mechanisms underlying effects on specific organ systems, we administered 0.2 or 0.8 mg/kg of dexamethasone to pregnant rats on gestational days 17, 18, and 19 and assessed th ... Full text Link to item Cite