Effect of antivitamin B6 on regional GABA metabolism in mouse brain and its relation to convulsions.

Publisher Website
Google Scholar
Abstract
The effects of administration of DL-penicillamine (PeA), thiosemicarbazide (TSC), semicarbazide-HCl (SC) as convulsants and pyridoxine (PN) as anticonvulsant on GABA content, glutamic acid decarboxylase (GAD) and GABA transaminase (GABA-T) activities in cerebral cortex, striatum, diencephalon, mesencephalon, cerebellum and pons/medulla were investigated. The onset of convulsions induced by these convulsants coincides with the fall in GABA content and GAD activity in the mesencephalon area and the cessation of the convulsions by PN supplement coincides with the recovery in both the parameters. Aminooxyacetic acid (AOAA), a potent GABA-elevating agent showed an anticonvulsant property against convulsion by TSC for several hours after the injection of AOAA, but lost this property 16 h after the treatment. The TSC administration 16 h after the AOAA pretreatment significantly decreased the GABA content in all the regions, particularly in the mesencephalon and diencephalon areas, which were elevated by the AOAA pretreatment, together with its ability to induce convulsion. The critical drop of GABA level from a plateau to another lower level following the decrease of GAD activity in the mesencephalon area is an important factor in the induction of convulsion.