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Research ArticleArticle

Zinc Inhibition of γ-Aminobutyric AcidA Receptor Function Is Decreased in the Cerebral Cortex during Pilocarpine-Induced Status Epilepticus

Pradeep K. Banerjee, Richard W. Olsen and O. Carter Snead III
Journal of Pharmacology and Experimental Therapeutics October 1999, 291 (1) 361-366;
Pradeep K. Banerjee
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Richard W. Olsen
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O. Carter Snead III
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Abstract

Functional modulation of γ-aminobutyric acidA(GABAA) receptors by Zn2+, pentobarbital, neuroactive steroid alphaxalone, and flunitrazepam was studied in the cerebral cortex and cerebellum of rats undergoing status epilepticus induced by pilocarpine. Under control conditions, Zn2+ dose-dependently inhibited muscimol-stimulated uptake of 36Cl− in cortical and cerebellar membranes. However, Zn2+ inhibition of stimulated36Cl− uptake was selectively decreased in the cortex (but not in the cerebellum) 1 to 2 h after the onset of status epilepticus. This loss of Zn2+ response in the cortex appeared to be selective to Zn2+ only, because pentobarbital-, alphaxalone-, or flunitrazepam enhancement of muscimol-stimulated 36Cl− uptake did not change in this brain region either at 1 or 2 h after seizures. Because this loss of Zn2+ response in the cortex was apparent only about 1 h after the onset of status epilepticus but not earlier, we tested whether status epilepticus was critical for the development of the loss of Zn2+ response. We found that, in rats where status epilepticus was terminated by diazepam within 30 min after seizure onset, Zn2+ response was preserved in the cortex. These findings suggest that continuous seizures of pilocarpine-induced status epilepticus caused a rapid and selective decrease in Zn2+ inhibition of GABAA receptor function in the cortex. The possible relevance of such rapid seizure-induced GABAA receptor plasticity in the cerebral cortex is discussed.

Footnotes

  • Send reprint requests to: Dr. O. Carter Snead III, Division of Neurology, Hospital for Sick Children, 555 University Ave., Toronto, Ontario M5G 1X8, Canada. E-mail:csnead{at}sickkids.on.ca

  • ↵1 This work was supported by the Brain and Behavior Program, Division of Neurology, Hospital for Sick Children, Toronto

  • Abbreviations:
    GABAA
    γ-aminobutyric acidA
    EEG
    electroencephalogram
    • Received April 23, 1999.
    • Accepted July 5, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 291 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 291, Issue 1
1 Oct 1999
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Research ArticleArticle

Zinc Inhibition of γ-Aminobutyric AcidA Receptor Function Is Decreased in the Cerebral Cortex during Pilocarpine-Induced Status Epilepticus

Pradeep K. Banerjee, Richard W. Olsen and O. Carter Snead
Journal of Pharmacology and Experimental Therapeutics October 1, 1999, 291 (1) 361-366;

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Research ArticleArticle

Zinc Inhibition of γ-Aminobutyric AcidA Receptor Function Is Decreased in the Cerebral Cortex during Pilocarpine-Induced Status Epilepticus

Pradeep K. Banerjee, Richard W. Olsen and O. Carter Snead
Journal of Pharmacology and Experimental Therapeutics October 1, 1999, 291 (1) 361-366;
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