[Effects of repeated treatment with electroconvulsive shock or imipramine on [3H]prazosin binding sites in the rat frontal cortex].

Two subtypes (alpha 1A and alpha 1B) of alpha 1-adrenoceptors have been defined on the basis of radioligand binding studies with 2-(2,6-dimethoxyphenoxyethyl)-1,4-benzodioxane (WB4101). In contrast, functional studies with blood vessels have proposed another subclassification, where the alpha 1-adrenoceptors can be classified into putative two (alpha 1H and alpha 1L) or three (alpha 1H, alpha 1L and alpha 1N) subtypes. The present study was performed to elucidate the effects of repeated treatment with electroconvulsive shock (ECS) or imipramine on the subtypes of alpha 1-adrenoceptors. The density of the alpha 1H binding sites (including alpha 1A and alpha 1B binding sites) in the frontal cortex was increased by repeated treatment with ECS but decreased by imipramine. These treatments did not change the density of alpha 1L binding sites. These results indicated that repeated treatment with ECS and imipramine had different effects on the alpha 1H binding sites in the rat frontal cortex. In addition, the effects of antipsychotic drugs, antidepressant drugs and calcium channel antagonists on [3H]prazosin binding were studied. The order of inhibition of [3H]prazosin binding was: antipsychotic drugs (1.4-4.2 nM) > antidepressant drugs (69-116 nM) > calcium channel antagonists. The calcium channel antagonists, verapamil (720 nM), diltiazem (4.3 microM) and nicardipine (75 microM) were weakly bound. These results suggested that the antimanic effects of calcium channel antagonists were not associated with inhibition of alpha 1-adrenoceptors.