The selective inhibition of hippocampal glutamic acid decarboxylase in zinc-induced epileptic seizures.
The intracerebroventricular administration of Zn2+ (0.3 mumol/10 microliters) 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 gamma-aminobutyric acid (0.4 mumol/10 microliters). 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 mumols 14CO2 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.
D000818:Animals; D002262:Carboxy-Lyases / Q000037:antagonists & inhibitors*; D005968:Glutamate Decarboxylase / Q000037:antagonists & inhibitors*; D006624:Hippocampus / Q000201:enzymology*; D008297:Male; D011732:Pyridoxal Phosphate / Q000032:analysis; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000139:chemically induced / Q000201:enzymology*; D015032:Zinc / Q000494:pharmacology*
D011732:Pyridoxal Phosphate; D002262:Carboxy-Lyases; D005968:Glutamate Decarboxylase; D015032:Zinc