Abstract
Resting tremor and hypokinesia of unilateral limbs were produced in monkeys after making a lesion in the mesencephalic tegmentum. The administration of L-dopa or dopamine agonists relieved them and followingly induced dyskinesias. The same effects were produced by the direct injection of dopamine or its agonists into the dorsomedial part of caudate nucleus ipsilateral to the lesion, where spiroperidol binding to the D2 receptor was increased in the affinity. These results suggest that denervation supersensitivity at the post-synaptic D2 receptor is a basic condition for the development of dyskinesias, though they were slightly suppressed by the intracaudate injection of GABA, serotonin and met-enkephalin.