Effect of chronic imipramine or baclofen on GABA-B binding and cyclic AMP production in cerebral cortex.
Long-term (14 days) treatment of mice with the antidepressant drug imipramine increased the number of GABA-B receptors in the cerebral cortex and also led to an increase in the potentiation of norepinephrine-induced cAMP accumulation by baclofen (a GABA-B agonist) in cortical slices. Chronic baclofen treatment decreased both of these measures. These results suggest that previous evidence of increased GABA-B binding by antidepressants is coupled to a functional increase in adenylate cyclase activity, but that the mechanism responsible for this effect is not due simply to direct GABA-B receptor stimulation.
D000818:Animals; D001418:Baclofen / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D000242:Cyclic AMP / Q000096:biosynthesis*; D007099:Imipramine / Q000494:pharmacology*; D008297:Male; D051379:Mice; D009638:Norepinephrine / Q000494:pharmacology; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D000242:Cyclic AMP; D001418:Baclofen; D007099:Imipramine; D009638:Norepinephrine