GABAB receptors and norepinephrine-stimulated cAMP production in rat brain cortex.
The ability of GABAergic compounds to influence cAMP accumulation in rat brain cortex was examined. It was found that GABAB receptor agonists such as GABA, baclofen, and kojic amine potentiate the cAMP response in cerebral cortex during exposure to norepinephrine. Isoguvacine and THIP, selective GABAA receptor agonists, did not demonstrate this effect. The response to baclofen was stereoselective, with virtually all activity residing in the (-)isomer. Bicuculline methiodide had no effect on the agonist-induced potentiation and the rank order of potency for GABAB agonists to potentiate the cAMP response is identical to their rank order of potency in the GABAB binding assay. These data suggest that GABAB receptors are capable of influencing the brain cyclic nucleotide system.
D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects / Q000502:physiology*; D000242:Cyclic AMP / Q000096:biosynthesis*; D004347:Drug Interactions; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*; D011753:Pyrones / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011956:Receptors, Cell Surface / Q000502:physiology*; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D011753:Pyrones; D011956:Receptors, Cell Surface; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; C018990:kojic amine; D000242:Cyclic AMP; D001418:Baclofen; D009638:Norepinephrine