Modulation of electroconvulsive treatment induced beta-adrenergic down-regulation by previous chronic imipramine administration: the involvement of protein kinase C.

To test how previous treatment with imipramine affects the action of electroconvulsive shock (ECS) on cortical beta-adrenergic system, male Wistar rats received imipramine, 10 mg/kg b.i.d. for two weeks, followed by 8 days of ECS, and 24 h after the last shock the responsiveness of beta-adrenoceptor system was tested by measuring cyclic AMP formation in cortical slices after exposure to noradrenaline or isoproterenol. To assess the possible role of protein kinase C, the same responses were measured in the presence of a protein kinase C activator, 12-O-tetradecanoyl-phorbol 13-acetate (TPA). ECS alone was found more effective in inducing beta-adrenergic-down-regulation than imipramine, and tended to produce stronger effect when given after chronic imipramine. In contrast to imipramine, which effectively inhibited TPA-induced potentiation of the action of isoproterenol, ECS strongly facilitated it. However, administrated after chronic treatment with imipramine, ECS did not change the potentiation. The results suggest that effects of ECS are slightly modified, but not inhibited by previous administration of imipramine.