The Involvement of the Superior Colliculus and Midbrain Reticular Formation in the Expression of Circling Behaviour

Abstract

Unilateral 6-hydroxydopamine (6OHDA) lesions of the nigrostriatal pathway resulted in contraversive rotation to apomorphine and ipsiversive rotation to amphetamine. Electrolytic lesioning of the nucleus reticularis gigantocellularis or kainic acid lesions of the nucleus tegmenti pedunculopontis on the same side as the 6OHDA lesion did not reduce apomorphine- or amphetamine-induced circling. Unilateral or bilateral electrolytic lesions of the rostral and caudal medial superior colliculus or a unilateral lesion of the deep lateral superior colliculus did not reduce apomorphine- or amphetamine-induced rotation in 6OHDA lesioned animals. An electrolesion of the angular complex (periaqueductal grey and adjacent reticular formation) on the same side as the 6OHDA lesion reduced apomorphine-induced circling and increased amphetamine-induced circling. Bilateral electrolesions of the angular complex reduced both apormophine- and amphetamine-induced rotation. The decrease in rotation was due to a loss of postural asymmetry while locomotor hyperactivity was maintained. A unilateral kainic acid lesion of the angular complex alone caused weak ipsiversive rotation which was enhanced by apomorphine and amphetamine. When a unilateral kainic acid lesion of the angular complex was made on the same side as a prior 6OHDA lesion, both apomorphine and amphetamine induced ipsiversive rotation. Unilateral injection of muscimol into the angular complex caused ipsiversive rotation which reversed the contraversive rotation elicited either by unilateral injection of muscimol into substantia nigra or by apomorphine administration to rats with a prior 6OHDA lesion, on the same side. The area of the angular complex is critically involved in the mediation of drug-induced circling in unilaterally 6OHDA lesioned rats and in particular the postural component.