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gamma-Aminobutyric acid(A) neurotransmission and cerebral ischemia.

Publication ,  Journal Article
Schwartz-Bloom, RD; Sah, R
Published in: J Neurochem
April 2001

In this review, we present evidence for the role of gamma-aminobutyric acid (GABA) neurotransmission in cerebral ischemia-induced neuronal death. While glutamate neurotransmission has received widespread attention in this area of study, relatively few investigators have focused on the ischemia-induced alterations in inhibitory neurotransmission. We present a review of the effects of cerebral ischemia on pre and postsynaptic targets within the GABAergic synapse. Both in vitro and in vivo models of ischemia have been used to measure changes in GABA synthesis, release, reuptake, GABA(A) receptor expression and activity. Cellular events generated by ischemia that have been shown to alter GABA neurotransmission include changes in the Cl(-) gradient, reduction in ATP, increase in intracellular Ca(2+), generation of reactive oxygen species, and accumulation of arachidonic acid and eicosanoids. Neuroprotective strategies to increase GABA neurotransmission target both sides of the synapse as well, by preventing GABA reuptake and metabolism and increasing GABA(A) receptor activity with agonists and allosteric modulators. Some of these strategies are quite efficacious in animal models of cerebral ischemia, with sedation as the only unwanted side-effect. Based on promising animal data, clinical trials with GABAergic drugs are in progress for specific types of stroke. This review attempts to provide an understanding of the mechanisms by which GABA neurotransmission is sensitive to cerebral ischemia. Furthermore, we discuss how dysfunction of GABA neurotransmission may contribute to neuronal death and how neuronal death can be prevented by GABAergic drugs.

Duke Scholars

Published In

J Neurochem

DOI

ISSN

0022-3042

Publication Date

April 2001

Volume

77

Issue

2

Start / End Page

353 / 371

Location

England

Related Subject Headings

  • gamma-Aminobutyric Acid
  • Synaptic Transmission
  • Receptors, GABA-A
  • Reactive Oxygen Species
  • Rats
  • Rabbits
  • Neuroprotective Agents
  • Neurons
  • Neurology & Neurosurgery
  • Models, Animal
 

Citation

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Schwartz-Bloom, R. D., & Sah, R. (2001). gamma-Aminobutyric acid(A) neurotransmission and cerebral ischemia. J Neurochem, 77(2), 353–371. https://doi.org/10.1046/j.1471-4159.2001.00274.x
Schwartz-Bloom, R. D., and R. Sah. “gamma-Aminobutyric acid(A) neurotransmission and cerebral ischemia.J Neurochem 77, no. 2 (April 2001): 353–71. https://doi.org/10.1046/j.1471-4159.2001.00274.x.
Schwartz-Bloom RD, Sah R. gamma-Aminobutyric acid(A) neurotransmission and cerebral ischemia. J Neurochem. 2001 Apr;77(2):353–71.
Schwartz-Bloom, R. D., and R. Sah. “gamma-Aminobutyric acid(A) neurotransmission and cerebral ischemia.J Neurochem, vol. 77, no. 2, Apr. 2001, pp. 353–71. Pubmed, doi:10.1046/j.1471-4159.2001.00274.x.
Schwartz-Bloom RD, Sah R. gamma-Aminobutyric acid(A) neurotransmission and cerebral ischemia. J Neurochem. 2001 Apr;77(2):353–371.
Journal cover image

Published In

J Neurochem

DOI

ISSN

0022-3042

Publication Date

April 2001

Volume

77

Issue

2

Start / End Page

353 / 371

Location

England

Related Subject Headings

  • gamma-Aminobutyric Acid
  • Synaptic Transmission
  • Receptors, GABA-A
  • Reactive Oxygen Species
  • Rats
  • Rabbits
  • Neuroprotective Agents
  • Neurons
  • Neurology & Neurosurgery
  • Models, Animal