• 1 January 1984
    • journal article
    • research article
    • Vol. 25 (1), 24-28
Abstract
Baclofen and GABA inhibit basal adenylate cyclase activity in brain of rat. The response is mediated through the GABAB receptor, and the rank order of potency for agonists is (-)-baclofen (EC50 = 4 .mu.M) > GABA (EC50 = 17 .mu.M) > muscimol > (+)-baclofen. GABAA agonists are not effective inhibitors of cyclase activity. The response is bicuculline-insensitive, and diazepam does not modify the GABA or (-)-baclofen inhibition of adenylate cyclase. Studies with neurologically mutant mice correlated a loss in GABAB receptor-mediated inhibition of cyclase with a loss in cerebellar granule cells. The GABAB receptor is negatively coupled to adenylate cyclase in various brain areas, and, in the cerebellum, a granule cell localization of this activity, is suggested.