| Abstract: | Contralateral rotation evoked by electrical stimulation of the left substantia nigra was studied in rats before and after electrolytic or 6-hydroxydopamine (6-OHDA) lesions of the lateral hypothalamus. Electrolytic lesions (2 mA DC, 15 sec) which produced mean ipsilateral striatal dopamine depletion of 58% significantly reduced the rotation at 2 h to 14 days postlesion. 6-OHDA (8 μg in 4 μl) which produced mean ipsilateral striatal dopamine depletion of 93% significantly increased the rotation at 3 to 14 days postlesion. Haloperidol 0.1 and 0.5 mg/kg i.p. partially reduced rotation in both control and lesioned rats in a dose-related manner. Control and lesioned rats showed no sognificant differences in haloperidol sensitivity. If stimulus induced rotation were mediated by activation of dopaminergic neurons, one would have expected lesion effects in the present experiments to parallel those on rotation caused by pharmacologically evoked release of dopamine. The lesion effects we obtained on stimulus induced rotation, however, parallel those on rotation evoked by the predominantly directly acting dopamine agonist, apomorphine, rather than those on rotation evoked by the indirect (presynaptic) action of amphetamine. We suggest that contralateral rotation evoked by electrical stimulation of the substantia nigra may reflect direct activation of neurons postsynaptic to the dopaminergic nigrostriatal neurons. |
