Relationship between .GAMMA.-aminobutyric acid metabolism and antivitamin B6-induced convulsions.

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Abstract
The correlation between the .gamma.-aminobutyric acid (GABA) metabolism and convulsions by some vitamin B6 antagonists, DL-penicillamine (PeA), hydrazine (Hyd) and thiosemicarbazide (TSC), were investigated. Glutamic acid decarboxylase (GAD) and .gamma.-aminobutyric acid transaminase (GABA-T) activities were inhibited during convulsions by 3 antagonists, and GABA content was not changed by PeA, increased by Hyd and decreased by TSC in mice whole brain. In subcellular fractions of brain, GAD activity was inhibited and GABA content decreased in synaptosomes during convulsions by the 3 drugs. Aminooxyacetic acid (AOAA), a potent GABA-elevating agent, showed an anticonvulsant property against convulsions by TSC for several hours after the injection of AOAA, but lost this property 16 h after treatment. During the convulsions by TSC 16 h after the AOAA-pretreatment, the GABA content in synaptosomes was less than that from the group treated with AOAA alone, though its GABA level was higher than the normal level. The GABA content and GAD activity in synaptosomes might be deeply associated with convulsions by B6 antagonists.