strychnine and gamma-aminobutyric-acid-cetyl-ester

The effect of piracetam on the electrophysiological and biochemical characteristics of the GABA system was studied and compared to that of cethyl ether of GABA (CEGABA). It was shown that piracetam (250-500 mg/kg) enhances the test response depression in the primary response recovery cycle and produces synchronization of the ECoG of the sensomotor cortex similarly to the previously described GABA-positive substances. The synchronizing effects of piracetam are retained upon isolation of the cortex and can be removed by bicucullin (rather than by strychnine) applied to the cortex. Piracetam decreases the GABA content in the brain cortex and inhibits the activity of glutamate decarboxylase. Analogous effect is exerted by CEGABA. A conclusion is drawn that GABA-ergic processes get potentiated under the effect of both the drugs. The selectivity of piracetam effects as to the cortical GABA-ergic inhibitory systems is likely to be the reason for the absence in the drug of anticonvulsant effect inherent in GABA mimetics with more generalized effects (CEGABA, muscimol).

Topics: Animals; Bicuculline; Cats; Cerebral Cortex; Electroencephalography; GABA Antagonists; gamma-Aminobutyric Acid; Male; Piracetam; Pyrrolidinones; Rats; Rats, Inbred Strains; Receptors, Drug; Strychnine