ANATOMICAL AND FUNCTIONAL EVIDENCE FOR LESION-SPECIFIC SPROUTING OF CORTICOSTRIATAL INPUT IN THE ADULT-RAT

Previous studies in our laboratory have shown that cortical lesions in duced by thermocoagulation of pial blood vessels, but not by acute asp iration, result in 1) the preservation of control levels of the growth -associated protein (GAP)-43 and 2) a prolonged increase in neurotrans mitter gene expression in the denervated dorsolateral striatum. We hav e examined whether corticostriatal projections from the spared homotyp ic contralateral cortex contribute to these effects. Adult rats receiv ed either a thermocoagulatory or aspiration lesion of the cerebral cor tex and, after 30 days, received an injection of the anterograde trace r, Fluoro-Ruby, in the contralateral homotypic cortex. Rats were kille d 7 days later, and labeled fibers were examined with fluorescence mic roscopy in the ipsilateral and contralateral striata. Ipsilateral cort icostriatal projections were detected in lesioned and unlesioned rats. Numerous labeled fibers were detected in the contralateral striatum o f thermocoagulatory-lesioned but not aspiration-lesioned or control an imals, suggesting that contralateral cortical neurons may undergo axon al sprouting in the denervated striatum following a thermocoagulatory lesion of the cortex. To determine whether contralateral corticostriat al fibers play a role in the changes in striatal gene expression induc ed by the thermocoagulatory lesions, the effects of aspiration lesions , as well as unilateral and bilateral thermocoagulatory lesions of the cortex were compared. Confirming previous results, striatal enkephali n mRNA levels were increased after a unilateral thermocoagulatory lesi on. However, they were unchanged after aspiration or bilateral thermoc oagulatory lesions, suggesting that sprouting or overactivity of contr alateral corticostriatal input contributes to the increase seen after unilateral thermocoagulatory lesions. (C) 1996 Wiley-Liss, Inc.