Abstract
The interaction of allylglycine (administered intraperitoneally, intraventricularly and intranigrally) with the γ-aminobutyric acid system was studied in a number of rat brain regions. The effects of allylglycine appeared to result from reduced availability of brain γ-aminobutyric acid through inhibition of glutamate decarboxylase activity. Allylglycine was a more effective inhibitor of glutamate decarboxylase in vivo than in vitro, and could be metabolized to 2-keto-pent-4-enoic acid. Sublethal doses of intraventricular allylglycine had no effect on γ-aminobutyric acid metabolism. Intranigral allylglycine initially produced contralateral circling behaviour accompanied by elevated dopamine turnover in the ipsilateral striatum— seizure activity was subsequently noted. Observed actions of allylglycine probably result from the combined actions of the parent amino acid and the keto-acid metabolite.
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