The selective inhibition of hippocampal glutamic acid decarboxylase in zinc-induced epileptic seizures |
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Authors: | Masatoshi Itoh MD Manuchair Ebadi |
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Institution: | (1) Department of Pharmacology, The University of Nebraska College of Medicine, 42nd Street and Dewey Avenue, 68105 Omaha, Nebraska;(2) Present address: Department of Neuropsychiatry, Faculty of Medicine, Kyushu University, 60, Maidashi 3-1-1, 812 Fukuoka, Japan |
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Abstract: | The intracerebroventricular administration of Zn2+ (0.3 mol/10 l) 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 -aminobutyric acid (0.4 mol/10 l). 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 mol14CO2 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. |
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