The effects of γ‐butyrolactone (GBL) and picrotoxin on both the post‐mortem and amino‐oxyacetic acid (AOAA) induced accumulations of γ‐aminobutyric acid (GABA) were examined in rats. GBL produced a marked dose‐dependent decrease in AOAA‐induced GABA accumulation in caudate. globus pallidus, cerebellar and cerebral cortices. The cingulate cortex showed the greatest response to GBL treatment; subanesthetic doses completely blocked the effect of AOAA. Picrotoxin increased the AOAA‐induced accumulation of GABA in parietal, entorhinal and cerebellar cortices, and had no significant effect in pyriform or cingulate cortices. Neither drug significantly altered the post‐mortem accumulation of GABA. Results suggest that picrotoxin, a GABA antagonist and convulsant drug, causes an increase in GABA synthesis in vivo. The apparent decrease in GABA synthesis following GBL treatment was greater than that observed with anesthetic doses of chloral hydrate and was not blocked by picrotoxin. Alterations in the activity of GABA neurons, cerebral glucose metabolism and GAD activity may contribute to the apparent decrease in in vivo GABA synthesis caused by GBL.
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Peričić et al. (1978) studied this question.
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