The selective inhibition of hippocampal glutamic acid decarboxylase in zinc-induced epileptic seizures

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Abstract
The intracerebroventricular administration of Zn2+ (0.3 μmol/10 μl) causes epileptic seizures characterized by running fits, jumping, vocalization, fasiculation of facial muscles, myoclonic movements of the limbs and tonic-clonic convulsions. These episodes are blocked or reversed by γ-aminobutyric acid (0.4 μmol/10 μl). When assayed under conditions where pyridoxal phosphate was not added, the activity of glutamic acid decarboxylase decreased significantly in hippocampus from 18.9 to 15.3 and 9.7 μmol14CO2 formed/gram proteins/20 min, 15 and 30 min following administration of Zn2+. The inhibition of glutamic acid decarboxylase by Zn2+ was selective occurring only in hippocampus and not in the hypothalamus, amygdala, caudate or thalamus. The inhibition of glutamic acid decarboxylase was not due to a reduction in the concentration of endogenous pyridoxal phosphate which remained unaltered in hippocampus following Zn2+ administration.