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Swim Stress Increases the Potency of Glycine at the N ‐Methyl‐ d ‐Aspartate Receptor Complex
Author(s) -
Nowak Gabriel,
Redmond Anna,
McNamara Mairead,
Paul Ian A.
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.64020925.x
Subject(s) - nmda receptor , strychnine , glycine receptor , glycine , glutamatergic , behavioural despair test , potency , pharmacology , receptor , agonist , neuroscience , glutamate receptor , chemistry , antidepressant , biology , in vitro , biochemistry , amino acid , hippocampus
We have previously demonstrated that chronic administration of antidepressants results in a reduction in the potency of glycine to displace 5,7‐[ 3 H]dichlorokynurenic acid (5,7‐[ 3 H]‐DCKA) from the strychnine‐insensitive glycine recognition site of the NMDA receptor complex. We now report that exposure of rats to the forced swim test results in a 56% increase in the potency of glycine to displace 5,7‐[ 3 H]DCKA from frontal cortical homogenates. These data are consistent with the hypothesis that the forced swim test, a preclinical screen sensitive to acute administration of antidepressant drugs and NMDA receptor antagonists, also results in adaptation of the NMDA receptor complex. Moreover, these data lend further support to the hypothesis that glutamatergic pathways are involved in the neurobiological response to stress and, potentially, in the pathophysiology of depression.