RESUMO
Apomorphine induced locomotor activity was studied in Wistar rats treated with imipramine and haloperidol with the help of automated measuring devices. The control rats showed a biphasic response of hypomotility and sedation to low dose apomorphine, and hypermotility to high dose apomorphine. In chronic imipramine-treated rats, the hypomotility and sedative response to low dose apomorphine challenge was significantly attenuated (P less than 0.05), as compared to saline treated controls. A similar response was observed in the chronically haloperidol treated rats (P less than 0.01). However, there were no significant differences in motility responses to high dose apomorphine challenge between the control and experimental groups. These results suggest that presynaptic dopamine auto receptors may not be involved in mediating the loss of response to low dose apomorphine by chronic imipramine treatment. Imipramine being predominantly a monoamine uptake inhibitor and haloperidol a potent postsynaptic D-2 blocker, some indirect mechanisms may be involved in the loss of response to low dose apomorphine challenge.