Abstract
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.
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