Lesion of the cerebellar paravermis increases dopamine D1 receptor levels in the contralateral striatum.

Anatomical and biochemical findings have long suggested that a projection from the cerebellum to the basal ganglia exists, and recent findings proposed that the cerebellum influences glutamatergic striatal activity. We have previously shown that a complete, genetic, lack of Purkinje cells induces an upregulation of dopamine D1 receptors (DRD1) in the output of the basal ganglia, the substantia nigra pars reticulata. In this study, we produced a focal unilateral lesion in the cerebellar paravermal cortex and we studied the levels and distribution of dopamine receptors and transporters, with the use of in vitro receptor autoradiography. The lesion produced a statistically significant increase in DRD1 specific binding in the contralateral medial striatum and a bilateral decrease in dopamine transporter (DAT) levels in the dorsolateral striatum. Our finding of a DRD1 increase after disruption of the cerebellar corticonuclear projection suggests that the cerebellar output modulates the basal ganglia DRD1-mediated pathway.