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  • Title: Zinc inhibition of GABA-stimulated Cl- influx in rat brain regions is unaffected by acute or chronic benzodiazepine.
    Author: Li M, Rosenberg HC, Chiu TH.
    Journal: Pharmacol Biochem Behav; 1994 Nov; 49(3):477-82. PubMed ID: 7862697.
    Abstract:
    Zinc modulation of GABAA receptor function was studied using GABA-stimulated 36Cl- influx into microsacs prepared from rat cerebral cortex, cerebellum and hippocampus. Zinc (10-100 microM) did not affect the basal influx, but significantly inhibited GABA-stimulated 36Cl- influx. The inhibition appeared to be noncompetitive. Zinc produced differing degrees of inhibition of GABA-stimulated 36Cl- influx in different brain regions. The order of sensitivity to zinc inhibition of GABA-stimulated 36Cl- influx was hippocampus > cerebral cortex > cerebellum. These regional differences may reflect the structural heterogeneity of GABAA receptors among brain areas. Zinc inhibition was not affected by the short-term addition of three benzodiazepines, diazepam, bretazenil and triazolam. The effect of diazepam and bretazenil to potentiate GABA-stimulated 36Cl- influx was not affected by zinc, but the effect of triazolam was decreased by zinc. In brain tissue prepared from flurazepam-treated rats, there was no difference compared with controls in zinc inhibition of GABA-stimulated 36Cl- influx. The results indicate that the effects of zinc on the GABAA receptor are largely independent of drugs acting on the benzodiazepine binding site.
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