Abstract
In an excitotoxin animal model of Huntington's disease (HD), fetal striatal tissue transplants survive and grow in the host brain and reverse the behavioral, and, hence, functional deficits produced by the lesion. In the present study we found recovery of apomorphine-induced rotation behavior in unilateral excitotoxin-lesioned rats indicating that the transplant reverses this functional pharmacologic deficit induced by the lesion. It might, therefore, by expected that the transplanted fetal striatal tissue would possess similar pharmacological characteristics as the host striatum. However, autoradiographic localization of D 1 and D 2 dopamine receptors demonstrated that the transplanted tissue expressed relatively small numbers of these receptor subtypes. Furthermore, there was a relative deficit of [ 3H]forskolin binding to the stimulatory guanine nucleotide regulatory subunit/adenylate cyclase complex in the fetal striatal tissue transplants. Therefore, transplanted tissue which is neurochemically dissimilar to the host striatum is capable of reversing deficits in both drug-induced and spontaneous locomotor activity.
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