Document Detail

Exposure to novelty and forced swimming evoke stressor-dependent changes in extracellular GABA in the rat hippocampus.
MedLine Citation:
PMID:  17693036     Owner:  NLM     Status:  MEDLINE    
In the hippocampus, a brain structure critically important in the stress response, GABA controls neuronal activity not only via synaptic inhibition, but also via tonic inhibition through stimulation of extrasynaptic GABA receptors. The extracellular level of GABA may represent a major determinant for tonic inhibition and, therefore, it is surprising that its responsiveness to stress has hardly been investigated. To clarify whether hippocampal extracellular GABA levels change in response to acute stress, we conducted an in vivo microdialysis study in rats. We found that dialysate GABA levels respond to various neuropharmacological manipulations such as reuptake inhibition, elevated concentrations of K(+), tetrodotoxin and baclofen, indicating that a large proportion of hippocampal extracellular GABA depends on neuronal release and that GABA re-uptake plays a role in determining the extracellular levels of this neurotransmitter. Next, rats were exposed to a novel cage or to forced swimming in 25 degrees C water. Interestingly, these two stressors resulted in opposite effects. Novelty caused a fast increase in GABA (120% of baseline), whereas forced swimming resulted in a profound decrease (70% of baseline). To discriminate between the psychological and physical aspects (i.e. the effects on body temperature) of forced swimming, another group of animals was forced to swim at 35 degrees C. This stressor, like novelty, caused an increase in hippocampal GABA, suggesting a stimulatory effect of psychological stress. The effects of novelty could not be blocked by the corticotropin-releasing factor receptor antagonist D-Phe-CRF(12-41). These results are the first to demonstrate stressor-dependent changes in hippocampal extracellular GABA; an observation which may be of particular significance for GABAergic tonic inhibition of hippocampal neurons.
L de Groote; A C E Linthorst
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-08-10
Journal Detail:
Title:  Neuroscience     Volume:  148     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-09-24     Completed Date:  2008-01-11     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  794-805     Citation Subset:  IM    
Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Dorothy Hodgkin Building, Department of Clinical Science at South Bristol, University of Bristol, Whitson Street, Bristol BS1 3NY, UK.
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MeSH Terms
Body Temperature / physiology
Corticosterone / metabolism,  secretion
Corticotropin-Releasing Hormone / metabolism
Exploratory Behavior / physiology*
Extracellular Fluid / metabolism
Fear / physiology
GABA Agonists / pharmacology
Hippocampus / metabolism*
Neural Inhibition / physiology*
Neurons / metabolism*
Potassium / metabolism,  pharmacology
Rats, Wistar
Receptors, Corticotropin-Releasing Hormone / antagonists & inhibitors,  metabolism
Sodium Channel Blockers / pharmacology
Stress, Psychological / metabolism*,  physiopathology
Swimming / physiology
Synaptic Transmission / drug effects,  physiology
gamma-Aminobutyric Acid / metabolism*
Reg. No./Substance:
0/GABA Agonists; 0/Receptors, Corticotropin-Releasing Hormone; 0/Sodium Channel Blockers; 50-22-6/Corticosterone; 56-12-2/gamma-Aminobutyric Acid; 7440-09-7/Potassium; 9015-71-8/Corticotropin-Releasing Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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