36Cl- flux measurements on GABAA receptor-activated chloride exchange. Multiple mechanisms of the chloride channel inactivation.

Article date: 1989/8/15

PubMed ID: 2548512

Journal name: Biochemical pharmacology (ISSN: 0006-2952)


The technique of radiotracer 36Cl- influx in primary culture of rat cerebellar granule cells was applied to study the mechanism of inactivation of the GABAA receptor-activated chloride channel. During sustained application of GABA, muscimol and THIP the specific bicuculline-sensitive 36Cl- influx tends to decline with time. The sequence in decay half-time is GABA less than muscimol less than THIP. Diazepam accelerates the rate of decay of the peak response to GABA. (-)-Baclofen enhances the rate of decline of the response to muscimol in a dose-dependent manner. Treatment of the cells with pertussis toxin antagonized the effect of (-)-baclofen. It is concluded that rat neonatal cerebellar neurons maintained in tissue culture exhibit complex inactivation of the GABAA channel, indicating some interaction with the GABAB receptor system.

This document is available from: http://directlinks.cc/files/muscimol/2548512.pdf

Author List: Kardos J

Publication Types: Journal Article

Substances mentioned in the article: Chloride Channels; Chlorides; Membrane Proteins; Radioisotopes; Receptors, GABA-A; Virulence Factors, Bordetella; Muscimol; Chlorine; Pertussis Toxin; Baclofen; Diazepam;

Mesh terms: Animals; Baclofen/pharmacology; Cerebellum/metabolism; Chloride Channels; Chlorides/metabolism; Chlorine/metabolism; Diazepam/pharmacology; In Vitro Techniques; Membrane Proteins/metabolism; Muscimol/pharmacology; Neurons/metabolism; Pertussis Toxin; Radioisotopes; Rats; Receptors, GABA-A/physiology; Virulence Factors, Bordetella/pharmacology;

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