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

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Abstract

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 < muscimol < 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.

Original languageEnglish
Pages (from-to)2587-2591
Number of pages5
JournalBiochemical Pharmacology
Volume38
Issue number16
DOIs
Publication statusPublished - Aug 15 1989

ASJC Scopus subject areas

  • Biochemistry
  • Pharmacology

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