Abstract
A boiled extract of porcine cerebral cortex was fractionated on Sephadex G-75 and LH-20 followed by paper chromatography of the active fraction having inhibitory activity towards [3H]GABA binding to rat brain synaptic membranes. A ninhydrin-negative substance migrating more quickly than authentic GABA was identified as a copper-GABA complex. The complex inhibited specific [3H]GABA binding (IC50 approximately equal to 1 microM) and antagonized the anticonvulsant effect exerted by intraamygdaloid injection of diazepam. The effect of a synthetic copper-GABA complex was compared and found to be similar to the endogenous complex. Cu2+ alone has no affinity for the GABA recognition site but antagonizes the anticonvulsant effect of diazepam. Therefore, Cu2+ is suggested to be the pharmacologically active principle of the endogenous substance. Cu2+ does not seem to function via the recognition site of the GABA receptor.
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