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Inhibition of GABA release from slices prepared from several brain regions of rats at various times following a convulsion
Author(s) -
Green A. Richard,
Minchin Michael C.W.,
Vincent Nigel D.
Publication year - 1987
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1987.tb11289.x
Subject(s) - convulsion , striatum , endogeny , hippocampus , chemistry , electroconvulsive shock , cerebral cortex , inhibitory postsynaptic potential , gamma aminobutyric acid , cortex (anatomy) , neuroscience , medicine , endocrinology , pharmacology , biology , biochemistry , receptor , dopamine , epilepsy
1 A method is described for the measurement of the K + ‐evoked release of endogenous γ‐aminobutyric acid (GABA) from slices of rat cortex, hippocampus and striatum. 2 In tissue prepared 30 min following an electroconvulsive shock, K + ‐evoked GABA release (above basal release) was inhibited by 45% in cortex, 50% in hippocampus and 75% in striatum. A similar inhibition of release was observed with slices prepared from rats in which a convulsion had been induced by flurothyl. There was no change in spontaneous (basal) release following either procedure. 3 An inhibition of K + ‐evoked endogenous GABA release was also seen in tissue prepared 4 min postictally but not 2 h after the seizure. 4 No difference was observed in the release of [ 3 H]‐GABA from preloaded cortical slices prepared from rats given a single electroconvulsive shock. 5 It is proposed that a convulsion results in an inhibition of GABA release and that this inhibition may in turn inhibit GABA synthesis as described in the preceding paper. 6 It is also proposed that changes in the endogenous releasable pool of GABA may not be detected by preloading slices with [ 3 H]‐GABA.