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Experimental injury resulted in a substantial decrease in dopamine type-1 (D<jats:sub>1<\/jats:sub>) and forskolin (adenylate cyclase) binding sites. In contrast, markers for dopamine type-2 (D<jats:sub>2<\/jats:sub>) sites and for dopamine uptake were unaffected in lesioned animals. Changes within dopaminergic pathways were variable, with reduction in binding being encountered mainly in components of the extrapyramidal motor system: caudate-putamen, -61%; globus pallidus, -64%; entopeduncular nucleus, -60%; and substantia nigra, -69%. Furthermore, the topography of D<jats:sub>1<\/jats:sub>receptor loss within the caudate-putamen was not uniform, with the greatest decrement in dorsolateral regions. Reduced D<jats:sub>1<\/jats:sub>versus D<jats:sub>2<\/jats:sub>receptor activation may underlie extrapyramidal movement disorders that appear as a consequence of perinatal hypoxic-ischemic insult. 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