Circling behaviour following unilateral kainic acid injections into rat striatum

Abstract

Unilateral injection of kainic acid (2,5–25 nmol) into rat anterior caudate-putamen induced dose-related circling behaviour. Kainic acid (10 nmol) consistently caused initial weak ipsiversive circling lasting 1 h followed by prolonged strong contraversive rotation lasting in excess of 10 h. Unilateral intrastriatal administration of L-glutamic acid, or of monosodium L-glutamate, to normal rats, or administration of monosodium L-glutamate to rats with extensive decortication, did not induce circling behaviour. The simultaneous unilateral injection of monosodium L-glutamate (1 μ mol) with kainic acid (10 nmol)_did not modify circling behaviour induced by kainic acid. However, extensive decortication greatly reduced circling induced by unilateral instratriatal kainic acid (10 nmol), an effect not reversed by the simultaneous administration of monosodium L-glutamate (1 μ mol). Unilateral 6-hydroxydopamine lesions of the left nigrostriatal pathway abolished the initial ipsiversive rotation and potentiated the subsequent contraversive rotation for u p to 4 h after intrastriatal injection of kainic acid (10 nmol). Peripheral administration of haloperidol (1 mg/kg i.p.) also abolished initial ipsiversive rotation and decreased the subsequent contraversive rotation. Electro-coagulation of the ipsilateral strio-nigral pathway prolonged the initial ipsiversive rotation produced by kainic acid, but markedly attenuated contraversive rotation. These findings suggest that circling induced by intrastriatal administration of kainic acid depends on intact corticostriate pathways, but it cannot be reproduced or modified by intrastriatal administration of glutamate. Kainic acid circling appears to be mediated via strio-nigral pathways, and to be modulated by dopaminergic function.