Abstract

Rats unilaterally lesioned with 6-hydroxydopamine to deplete striatal dopamine received daily injections of levodopa methyl ester in combination with benserazide. Delayed lesions in the subthalamic nucleus (Group 2) or entopeduncular nucleus and substantia nigra par reticulata (Group 3) were made, unilateral to the dopamine depletion. Apomorphine-induced rotation was significantly reduced in Group 2 versus sham-operated controls ( P<0.006) and in Group 3 versus Group 2 ( P<0.03). Results suggest that enhanced apomorphine-induced rotation in this model is mediated through both the striatopallidal and striatonigral pathway.

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