GABAB receptor activation inhibits CA2+-activated potassium channels in synaptosomes: Involvement of G-proteins

Maharaj K. Ticku, Angel Delgado

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

86Rb-efflux assay from preloaded synaptosomes of rat cerebral cortex was developed to study the effect of GABAB receptor agonist baclofen on Ca2+-activated K+-channels. Depolarization (100 mM K) of 86Rb-loaded synaptosomes in physiological buffer increased Ca2+-activated 86Rb-efflux by 400%. The 86Rb-efflux was blocked by quinine sulphate, tetraethylammonium, and La3+ indicating the involvement of Ca2+-activated K+-channels. (-)Baclofen inhibited Ca2+-activated 86Rb-efflux in a stereospecific manner. The inhibitory effect of (-)baclofen was mediated by GABAB receptor activation, since it was blocked by GABAB antagonist phaclofen, but not by bicuculline. Further, pertussis toxin also blocked the ability of baclofen or depolarizing action to affect Ca2+-activated K+-channels. These results suggest that baclofen inhibits Ca2+-activated K+-channels in synaptosomes and these channels are regulated by G-proteins. This assay may provide an ideal in vitro model to study GABAB receptor pharmacology.

Original languageEnglish (US)
Pages (from-to)1271-1276
Number of pages6
JournalLife Sciences
Volume44
Issue number18
DOIs
StatePublished - 1989

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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