Repeated imipramine and electroconvulsive shock increase alpha 1A-adrenoceptor mRNA level in rat prefrontal cortex.

alpha(1)-Adrenoceptors have been implicated in the mechanism of action of antidepressants, but their action on specific receptor subtypes was rarely reported. We compared now the action of two prototypic antidepressant treatments: repeated imipramine and electroconvulsive shock, on the expression of the alpha(1A)- and alpha(1B)-adrenoceptor mRNAs and on the receptor density in rats. The mRNA expression was assessed by Northern blot in the prefrontal cortex and the hippocampus, the receptor density was measured by [3H]prazosin binding in the total cerebral cortex and hippocampus. In the cortex, both treatments elevated the alpha(1A)-adrenoceptor mRNA and the expression of receptor protein. The expression of alpha(1B)-adrenoceptor mRNA remained unaffected. In contrast, in the hippocampus, the antidepressant treatments augmented the density of alpha(1A)-adrenoceptor protein without changing the level of its mRNA expression there. The results suggest that the alpha(1A)-adrenoceptor subtype is specifically involved in the mechanism of action of classical antidepressant treatments.