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γ‐Aminobutyric Acid Release from Synaptosomes Prepared from Rats Treated with Isonicotinic Acid Hydrazide and Gabaculine
Author(s) -
Wood J. D.,
Kurylo E.,
Lane R.
Publication year - 1988
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 - 10.1111/j.1471-4159.1988.tb02486.x
Subject(s) - chemistry , isonicotinic acid , hydrazide , aminobutyric acid , convulsant , pharmacology , synaptosome , gamma aminobutyric acid , anticonvulsant , biochemistry , potassium , biophysics , biology , receptor , neuroscience , organic chemistry , in vitro , epilepsy
The potassium‐stimulated release of γ‐aminobutyric acid (GABA) from synaptosomes was determined in preparations from control rats and from rats treated with a convulsant agent [isonicotinic acid hydrazide (INH)] and an anticonvulsant agent (gabaculine). INH treatment brought about a significant decrease in Ca 2+ ‐dependent release of GABA with no effect on Ca 2+ ‐independent release, whereas gabaculine caused an increase in Ca 2+ ‐independent release with no effect on Ca 2+ ‐dependent release of GABA. Thus, the anticonvulsant action of gabaculine was not a simple reversal of the effects of INH on GABA release. The results indicate that there are at least two pools of GABA in nerve endings and support the hypothesis that exogenous GABA is taken up first into a pool that supplies GABA for Ca 2+ ‐independent release and then is transferred to a second pool (Ca 2+ ‐dependent releasable), where it mixes with newly synthesized GABA.