Abstract

Unilateral application of γ-aminobutyric acid (GABA) antagonists on the motor cortex of conscious rats produces myoclonic movements. Paradoxically, the same behaviour can be observed with high concentrations of some GABA-transaminase (GABA-T) Inhibitors. Since the GABA conjugate homocarnosine is increased in the brain following GABA-T inhibition and since homocarnosine is known to displace [ 3H]-GABA from Its binding sites at high concentration, we investigated whether homocarnosine might explain the dyskinetic movements produced by these GABA-T inhibitors. We found that homocarnosine produces dyskinesia similar to that observed with GABA antagonists and GABA-T inhibitors when applied directly to the cortex. However, this property of homocarnosine is unlikely to be the basis of the dyskinetic effect of GABA-T Inhibitors since we found no relationship between brain homocarnoslne levels and the appearance of abnormal movements following GABA-T inhibition.

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