Graft-induced behavioral recovery in an animal model of Huntington disease.

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Abstract
Bilateral ibotenic acid lesions of the anteromedial neostriatum produce neuropathological and behavioral changes in rats that are characterized by locomotor hyperactivity and severe maze learning impairments, which can be viewed as analogous to changes seen in Huntington disease. Grafts of fetal striatal neurons, implanted either into the lesioned striatum or into the denervated globus pallidus, reduced both the learning impairments and the locomotor hyperactivity, probably via different mechanisms. The results demonstrate the capacity of neural implants for functional neuronal replacement and promotion of functional recovery after damage to a major telencephalic structure participating in complex cognitive and motoric behaviors.