Nature of receptors involved in apomorphine responses in pigeons

Abstract

Apomorphine provokes pecking and emesis in pigeons. These effects are mediated through activation of dopamine receptors. In the present paper the effect of apomorphine on the body temperature was studied and an attempt made to determine whether the receptors mediating pecking, emesis, thermoregulatory effects, etc. were similar or different in their transmitter reactivity.

Apomorphine was injected by either an intravenous or intracerebroventricular route. It produced dosedependent pecking and hypothermia. Pecking occurred in the form of a syndrome comprised of preening and visual exploratory movements of the head preceding and following a period of pecking. Large intraventricular doses produced emesis, vocalization, and opisthotonus. When apomorphine was injected intravenously, the dose required was smaller than that required by intraventricular route, suggesting that the receptors involved are located away from the ventricular surface. The reverse was true for hypothermia.

The effects of apomorphine were prevented by the dopamine receptor-blocking substance pimozide, but were unaffected by the adrenoceptor-blocking substances phenoxybenzamine and propranolol. Pecking alone was suppressed by 5-HT and facilitated by cyproheptadine.

The results indicate that the activation of dopamine receptors mediates the different apomorphine responses, of which only pecking is modulated by activation of tryptamine receptors.