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Male, Wistar rats were given a course of eight electroconvulsive shock seizures (ECS group) or matched handling (control group). They were then tested for locomotion and rearing (7 days post-ECS), for grooming and yawning (9 days post-ECS), and for immobility in the Porsolt test (7, 14 and 21 days post-ECS). Seven days post-seizure, the ECS group showed significantly more locomotion following intraperitoneal administration of apomorphine (0.2 mg/kg), but not following injections of amphetamine (1 mg/kg). Drug-induced rearing was not different in the ECS and control animals. Nine days post-seizure, the ECS group showed significantly more grooming induced by the D-1 dopamine receptor agonist, SKF 38393 (1 mg/kg), but no difference in the yawning induced by the D-2 dopamine receptor agonist, quinpirole (0.05 mg/kg). In the Porsolt test, immobility was decreased in the ECS animals at 7 and 14, but not at 21 days post-ECS. It is concluded that ECS increases activity in the dopaminergic systems of the rat brain for at least 1-2 weeks post-seizure. The beneficial effects of electroconvulsive therapy (ECT) may relate to these dopaminergic alterations.

In this study, the effect of cholinergic agents on imipramine antinociception in mice, in the formalin test, has been investigated. Intraperitoneal (i.p.) administration of different doses of imipramine (2.5, 5, 10, 20 and 30 mg/kg) or nicotine (0.25, 0.5, 0.75 and 1 mg/kg) induced a dose dependent antinociception in both the first and second phases of the formalin test in mice. The combination of imipramine with doses of 0.5 and 0.75 mg/kg of nicotine showed a potentiated response, in both phases of the test. However, neither hexamethonium (5 and 10 mg/kg), atropine (0.25 mg/kg) or mecamylamine (0.25 mg/kg) altered the antinociception induced by imipramine. It is concluded that nicotinic receptor activation but not the cholinergic muscarinic mechanism is involved in the imipramine-induced antinociception.

In this study, the effects of adrenoceptor agonists and antagonists on antinociception induced by imipramine in sciatic-nerve-ligated mice were investigated. The response of different doses of morphine, imipramine and adrenoceptor agonists and antagonists was examined 14 days after unilateral nerve-ligation in the hot-plate test. Intraperitoneal injection of different doses of morphine (3, 6 and 9 mg/kg), imipramine (10, 20 and 40 mg/kg), the alpha(2)-adrenoceptor agonist, clonidine (0.05, 0.1 and 0.2 mg/kg) or the alpha(1)-adrenoceptor agonist, phenylephrine (2, 4 and 8 mg/kg) induced dose-related antinociception in both intact and nerve-ligated mice. The antinociception induced by morphine but not that of imipramine, clonidine or phenylephrine, in nerve-ligated mice was significantly less than that induced in intact animals. Imipramine in combination with clonidine tends to induce a higher response, but the combination of imipramine with phenylephrine did not lead to significant potentiation. The alpha(2)-adrenoceptor antagonist, yohimbine, reduced the response induced by imipramine or imipramine plus clonidine in intact and nerve-ligated animals. However, the alpha(1)-adrenoceptor antagonist, prazosin, did not alter imipramine response. It may be concluded that imipramine induced antinociception in both intact and nerve-ligated mice through an alpha(2)-adrenoceptor mechanism(s).