Inhibition by lithium of beta-endorphin-induced psychomotor excitation in cats

Abstract

beta-Endorphin injected into the cerebral ventricles of unanesthetized cats produced dose-dependent and long-lasting restlessness, locomotion, stereotyped sideways movements of the head, vacant staring, apprehension and flight accompanied with mydriasis and tremor. The most impressive features of the psychomotor excitation were the locomotion and the sideways movements of the head. Intracerebroventricular nalorphine prevented the psychomotor excitation caused by intracerebroventricular beta-endorphin. Lithium chloride and lithium carbonate injected into the cerebral ventricles prevented and reversed the psychomotor excitation evoked by beta-endorphin similarly injected. In cats showing spontaneous locomotor activity, intracerebroventricular lithium chloride also suppressed this activity. It is suggested that beta-endorphin elicited psychomotor excitation by acting on central opiate receptors. However, the effect of lithium cannot be solely ascribed to an action on central opiate receptors and endogenous peptides. Since lithium affected the spontaneous as well as the beta-endorphin-induced locomotion, it may be supposed that the cation suppressed the ongoing input activity at central locomotion activity levels.