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Effects of Hypoxic-Ischemic Brain Damage on Dopaminergic Markers in the Neonatal Rat: A Regional Autoradiographic AnalysisDepartments of Neurology, Pediatrics, and Psychiatry, University of Utah School of Medicine, Salt Lake City, UT
Departments of Neurology, Pediatrics, and Psychiatry, University of Utah School of Medicine, Salt Lake City, UT Dopamine has been implicated as an endogenous substance that may mediate neuronal death after hypoxic-ischemic insult. Using semiquantitative autoradiography, we studied the effect of perinatal hypoxic-ischemic injury on dopamine binding sites in rat brain. Experimental injury resulted in a substantial decrease in dopamine type-1 (D1) and forskolin (adenylate cyclase) binding sites. In contrast, markers for dopamine type-2 (D2) 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 D1 receptor loss within the caudate-putamen was not uniform, with the greatest decrement in dorsolateral regions. Reduced D1 versus D2 receptor activation may underlie extrapyramidal movement disorders that appear as a consequence of perinatal hypoxic-ischemic insult. (J Child Neurol 1992;7:199-207).
Journal of Child Neurology, Vol. 7, No. 2,
199-207 (1992) This article has been cited by other articles:
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