Hyperalgesia

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  Subject Areas on Research

  • 5,6-EET is released upon neuronal activity and induces mechanical pain hypersensitivity via TRPA1 on central afferent terminals. 
  • A feed-forward spinal cord glycinergic neural circuit gates mechanical allodynia. 
  • A moldable sustained release bupivacaine formulation for tailored treatment of postoperative dental pain. 
  • A peptide c-Jun N-terminal kinase (JNK) inhibitor blocks mechanical allodynia after spinal nerve ligation: respective roles of JNK activation in primary sensory neurons and spinal astrocytes for neuropathic pain development and maintenance. 
  • Activation of metabotropic glutamate receptor 7 in spinal cord inhibits pain and hyperalgesia in a novel formalin model in sheep. 
  • Anti-PD-1 treatment impairs opioid antinociception in rodents and nonhuman primates. 
  • Antihyperalgesic effects of vanilloid-1 and bradykinin-1 receptor antagonists following spinal cord injury in rats. 
  • Astrocytic CX43 hemichannels and gap junctions play a crucial role in development of chronic neuropathic pain following spinal cord injury. 
  • B1 and TRPV-1 receptor genes and their relationship to hyperalgesia following spinal cord injury. 
  • Basal and carrageenan-induced pain behavior in Sprague-Dawley, Lewis and Fischer rats. 
  • Biochemical and pharmacological profile of a tetrasubstituted furanone as a highly selective COX-2 inhibitor. 
  • Bradykinin enhances AMPA and NMDA receptor activity in spinal cord dorsal horn neurons by activating multiple kinases to produce pain hypersensitivity. 
  • Bradykinin produces pain hypersensitivity by potentiating spinal cord glutamatergic synaptic transmission. 
  • Brain-derived neurotrophic factor-activated astrocytes produce mechanical allodynia in neuropathic pain. 
  • CACNG2 polymorphisms associate with chronic pain after mastectomy. 
  • Carbonic anhydrase-8 regulates inflammatory pain by inhibiting the ITPR1-cytosolic free calcium pathway. 
  • Catechol-O-methyltransferase inhibition increases pain sensitivity through activation of both beta2- and beta3-adrenergic receptors. 
  • Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4. 
  • Cell signaling and the genesis of neuropathic pain. 
  • Central immune overactivation in the presence of reduced plasma corticosterone contributes to swim stress-induced hyperalgesia. 
  • Choline attenuates inflammatory hyperalgesia activating nitric oxide/cGMP/ATP-sensitive potassium channels pathway. 
  • Chronic inflammatory pain leads to increased blood-brain barrier permeability and tight junction protein alterations. 
  • Connexin-43 induces chemokine release from spinal cord astrocytes to maintain late-phase neuropathic pain in mice. 
  • Cytokine mechanisms of central sensitization: distinct and overlapping role of interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha in regulating synaptic and neuronal activity in the superficial spinal cord. 
  • Different immune cells mediate mechanical pain hypersensitivity in male and female mice. 
  • Differential Inhibition of Nav1.7 and Neuropathic Pain by Hybridoma-Produced and Recombinant Monoclonal Antibodies that Target Nav1.7 : Differential activities of Nav1.7-targeting monoclonal antibodies. 
  • Differential effects of experimental central sensitization on the time-course and magnitude of offset analgesia. 
  • Disruption of ErbB receptor signaling in adult non-myelinating Schwann cells causes progressive sensory loss. 
  • ERK MAP kinase activation in superficial spinal cord neurons induces prodynorphin and NK-1 upregulation and contributes to persistent inflammatory pain hypersensitivity. 
  • ETAR and protein kinase A pathway mediate ET-1 sensitization of TRPA1 channel: A molecular mechanism of ET-1-induced mechanical hyperalgesia. 
  • Effects of nociceptin (13-17) in pain modulation at supraspinal level in mice. 
  • Endogenous tumor necrosis factor alpha (TNFalpha) requires TNF receptor type 2 to generate heat hyperalgesia in a mouse cancer model. 
  • Enhanced central thermal nociception in mildly depressed nonpatients and transiently sad healthy subjects. 
  • Epiregulin and EGFR interactions are involved in pain processing. 
  • Expression of PSD-95/SAP90 is critical for N-methyl-D-aspartate receptor-mediated thermal hyperalgesia in the spinal cord. 
  • Exteroceptive suppression periods and pericranial muscle tenderness in chronic tension-type headache: Effects of psychopathology, chronicity, and disability 
  • Extracellular caspase-6 drives murine inflammatory pain via microglial TNF-α secretion. 
  • Gabapentin Use in the Neonatal Intensive Care Unit. 
  • Gabapentin attenuates morphine tolerance through interleukin-10. 
  • Gait abnormalities and inflammatory cytokines in an autologous nucleus pulposus model of radiculopathy. 
  • Genetically determined P2X7 receptor pore formation regulates variability in chronic pain sensitivity. 
  • Human carbonic anhydrase-8 AAV8 gene therapy inhibits nerve growth factor signaling producing prolonged analgesia and anti-hyperalgesia in mice. 
  • Identifying local and descending inputs for primary sensory neurons. 
  • Impact of human CA8 on thermal antinociception in relation to morphine equivalence in mice. 
  • In vivo luminescence imaging of NF-κB activity and serum cytokine levels predict pain sensitivities in a rodent model of osteoarthritis. 
  • In vivo luminescent imaging of NF-κB activity and NF-κB-related serum cytokine levels predict pain sensitivities in a rodent model of peripheral neuropathy. 
  • Induction of CB1 cannabinoid receptor by inflammation in primary afferent neurons facilitates antihyperalgesic effect of peripheral CB1 agonist. 
  • Inhibition of mechanical allodynia in neuropathic pain by TLR5-mediated A-fiber blockade. 
  • Intrathecal administration of antisense oligonucleotide against p38α but not p38β MAP kinase isoform reduces neuropathic and postoperative pain and TLR4-induced pain in male mice. 
  • Involvement of Transient Receptor Potential Cation Channel Member A1 activation in the irritation and pain response elicited by skin-lightening reagent hydroquinone. 
  • Ionotropic and metabotropic receptors, protein kinase A, protein kinase C, and Src contribute to C-fiber-induced ERK activation and cAMP response element-binding protein phosphorylation in dorsal horn neurons, leading to central sensitization. 
  • Is Optogenetic Activation of Vglut1-Positive Aβ Low-Threshold Mechanoreceptors Sufficient to Induce Tactile Allodynia in Mice after Nerve Injury? 
  • Kinematic and dynamic gait compensations in a rat model of lumbar radiculopathy and the effects of tumor necrosis factor-alpha antagonism. 
  • L6 spinal nerve ligation produces prolonged development of mechanical allodynia and gradual increase of GFAP on ipsilateral dorsal horn. 
  • Lack of evidence for ectopic sprouting of genetically labeled Aβ touch afferents in inflammatory and neuropathic trigeminal pain. 
  • Light touch induces ERK activation in superficial dorsal horn neurons after inflammation: involvement of spinal astrocytes and JNK signaling in touch-evoked central sensitization and mechanical allodynia. 
  • Long-lasting delayed hyperalgesia after subchronic swim stress. 
  • Long-term male-specific chronic pain via telomere- and p53‑mediated spinal cord cellular senescence. 
  • Loss of NR1 subunit of NMDARs in primary sensory neurons leads to hyperexcitability and pain hypersensitivity: involvement of Ca(2+)-activated small conductance potassium channels. 
  • Lysophospholipids Contribute to Oxaliplatin-Induced Acute Peripheral Pain. 
  • Macrophage Toll-like Receptor 9 Contributes to Chemotherapy-Induced Neuropathic Pain in Male Mice. 
  • Mechanical hyperalgesia and reduced quality of life occur in people with mild knee osteoarthritis pain. 
  • Mechanistic contribution of CaV3.2 calcium channels to trigeminal neuralgia pathophysiology not clarified. 
  • Metastatic human breast cancer to the spine produces mechanical hyperalgesia and gait deficits in rodents. 
  • Microglia Promote Increased Pain Behavior through Enhanced Inflammation in the Spinal Cord during Repeated Social Defeat Stress. 
  • Microglia-mediated degradation of perineuronal nets promotes pain. 
  • Minocycline attenuates mechanical allodynia and expression of spinal NMDA receptor 1 subunit in rat neuropathic pain model. 
  • Modulation of activity and conduction in single dorsal column axons by kilohertz-frequency spinal cord stimulation. 
  • Mu Opioid Splice Variant MOR-1K Contributes to the Development of Opioid-Induced Hyperalgesia. 
  • Neonatal chronic hind paw inflammation alters sensitization to intradermal capsaicin in adult rats: a behavioral and immunocytochemical study. 
  • Neurokinin-1 receptor enhances TRPV1 activity in primary sensory neurons via PKCepsilon: a novel pathway for heat hyperalgesia. 
  • Neuropathic pain activates the endogenous kappa opioid system in mouse spinal cord and induces opioid receptor tolerance. 
  • Neuropathic pain is constitutively suppressed in early life by anti-inflammatory neuroimmune regulation. 
  • Nuclear factor-kappa B regulates pain and COMT expression in a rodent model of inflammation. 
  • Opioid-independent mechanisms supporting offset analgesia and temporal sharpening of nociceptive information. 
  • Orthopedic surgery modulates neuropeptides and BDNF expression at the spinal and hippocampal levels. 
  • PD-L1 inhibits acute and chronic pain by suppressing nociceptive neuron activity via PD-1. 
  • Paclitaxel-induced neuropathic hypersensitivity in mice: responses in 10 inbred mouse strains. 
  • Perspectives on the genetic basis of opioid-induced hyperalgesia. 
  • Phosphatidylinositol 3-kinase activates ERK in primary sensory neurons and mediates inflammatory heat hyperalgesia through TRPV1 sensitization. 
  • Phosphorylation of transcription factor CREB in rat spinal cord after formalin-induced hyperalgesia: relationship to c-fos induction. 
  • Protease-activated receptor 2 sensitizes the transient receptor potential vanilloid 4 ion channel to cause mechanical hyperalgesia in mice. 
  • Reduced GABA neurotransmission underlies hyperalgesia induced by repeated forced swimming stress. 
  • Reduction of spinal PGE2 concentrations prevents swim stress-induced thermal hyperalgesia. 
  • Repetitive hyperbaric oxygen treatment attenuates complete Freund's adjuvant-induced pain and reduces glia-mediated neuroinflammation in the spinal cord. 
  • Resolvin E1 inhibits neuropathic pain and spinal cord microglial activation following peripheral nerve injury. 
  • Rofecoxib [Vioxx, MK-0966; 4-(4'-methylsulfonylphenyl)-3-phenyl-2-(5H)-furanone]: a potent and orally active cyclooxygenase-2 inhibitor. Pharmacological and biochemical profiles. 
  • Role of mu-opioid and NMDA receptors in the development and maintenance of repeated swim stress-induced thermal hyperalgesia. 
  • Roles of inflammation, neurogenic inflammation, and neuroinflammation in pain. 
  • SHANK3 Deficiency Impairs Heat Hyperalgesia and TRPV1 Signaling in Primary Sensory Neurons. 
  • STING suppresses bone cancer pain via immune and neuronal modulation. 
  • Selective activation of cannabinoid CB(2) receptors suppresses spinal fos protein expression and pain behavior in a rat model of inflammation. 
  • Selective inhibition of JNK with a peptide inhibitor attenuates pain hypersensitivity and tumor growth in a mouse skin cancer pain model. 
  • Short small-interfering RNAs produce interferon-α-mediated analgesia. 
  • Sphygmomanometry-evoked allodynia in chronic pain patients with and without fibromyalgia. 
  • Spinal CCL2 Promotes Central Sensitization, Long-Term Potentiation, and Inflammatory Pain via CCR2: Further Insights into Molecular, Synaptic, and Cellular Mechanisms. 
  • Spinal injection of TNF-α-activated astrocytes produces persistent pain symptom mechanical allodynia by releasing monocyte chemoattractant protein-1. 
  • Stress-induced hyperalgesia is associated with a reduced and delayed GABA inhibitory control that enhances post-synaptic NMDA receptor activation in the spinal cord. 
  • Stress-induced muscle and cutaneous hyperalgesia: differential effect of milnacipran. 
  • Sustained stimulation of β2- and β3-adrenergic receptors leads to persistent functional pain and neuroinflammation. 
  • T-Cell Mediation of Pregnancy Analgesia Affecting Chronic Pain in Mice. 
  • The LURN Research Network Neuroimaging and Sensory Testing (NIST) Study: Design, protocols, and operations. 
  • The c-Jun N-terminal kinase 1 (JNK1) in spinal astrocytes is required for the maintenance of bilateral mechanical allodynia under a persistent inflammatory pain condition. 
  • The effect of intrathecal administration of glial activation inhibitors on dorsal horn BDNF overexpression and hind paw mechanical allodynia in spinal nerve ligated rats. 
  • The metabotropic glutamate receptor 5 negative allosteric modulator fenobam: pharmacokinetics, side effects, and analgesic effects in healthy human subjects. 
  • The selective metabotropic glutamate receptor 7 allosteric agonist AMN082 inhibits inflammatory pain-induced and incision-induced hypersensitivity in rat. 
  • Thrombospondin-4 contributes to spinal sensitization and neuropathic pain states. 
  • Tissue plasminogen activator contributes to morphine tolerance and induces mechanical allodynia via astrocytic IL-1β and ERK signaling in the spinal cord of mice. 
  • Toll-like receptor 4 contributes to chronic itch, alloknesis, and spinal astrocyte activation in male mice. 
  • Transient receptor potential vanilloid 4 mediates protease activated receptor 2-induced sensitization of colonic afferent nerves and visceral hyperalgesia. 
  • Transient receptor potential vanilloid-4 has a major role in visceral hypersensitivity symptoms. 
  • Upregulation of the voltage-gated sodium channel beta2 subunit in neuropathic pain models: characterization of expression in injured and non-injured primary sensory neurons. 
  • p38 MAPK activation by NGF in primary sensory neurons after inflammation increases TRPV1 levels and maintains heat hyperalgesia. 
  • p38 mitogen-activated protein kinase is activated after a spinal nerve ligation in spinal cord microglia and dorsal root ganglion neurons and contributes to the generation of neuropathic pain. 
  • β-arrestin-2 regulates NMDA receptor function in spinal lamina II neurons and duration of persistent pain. 
  • β2- and β3-adrenergic receptors drive COMT-dependent pain by increasing production of nitric oxide and cytokines. 
  • μ-Opioid Receptor Gene A118 G Variants and Persistent Pain Symptoms Among Men and Women Experiencing Motor Vehicle Collision. 
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  Keywords of People

  • Gunn, Michael Dee, Professor of Medicine, Integrative Immunobiology
  • Martucci, Katherine, Assistant Professor in Anesthesiology, Center for Cognitive Neuroscience