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Effect of Unilateral Perinatal Hypoxic‐Ischemic Brain Injury in the Rat on Dopamine D 1 and D 2 Receptors and Uptake Sites: A Quantitative Autoradiographic Study
Author(s) -
Przedborski Serge,
Kostic Vladimir,
JacksonLewis Vernice,
Cadet Jean Lud,
Burke Robert E.
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb06409.x
Subject(s) - putamen , dopamine , endocrinology , medicine , spiperone , dopaminergic , substantia nigra , sch 23390 , caudate nucleus , dopamine receptor , chemistry , lesion , biology , pathology
The effect of a unilateral perinatal hypoxic‐ischemic brain injury on dopamine D 1 and D 2 receptors and uptake sites was investigated in rats by using in vitro quantitative binding autoradiography, 2–3 weeks after the insult. We observed significant decreases in the B max and K D for [ 3 H]SCH 23390‐labeled D 1 and in the B max for [ 3 H]spiperone‐labeled D 2 receptors in the lesioned caudate‐putamen in rats with moderate brain injury (visible loss in hemispheric volume ipsilateral to the injury) compared with the nonlesioned contralateral caudate‐putamen or with control rats. Changes in [ 3 H]SCH 23390 and [ 3 H]spiperone binding predominated in the dorsolateral part of the lesioned caudate‐putamen. Pronounced reduction in [ 3 H]SCH 23390 binding was also observed in the substantia nigra pars reticulata on the side of the lesion. In contrast, we did not observe any significant change in B max or K D for [ 3 H]mazindol‐labeled dopamine uptake sites. Similarly, no significant changes in the levels of dopamine or its metabolites were found on the side of the lesion. The observed reductions in striatal dopamine D 1 and D 2 receptors are a reflection of striatal cell loss induced by the hypoxic‐ischemic injury. The absence of changes in [ 3 H]mazindoI binding or dopamine levels in the lesioned caudate‐putamen indicates that the dopaminergic presynaptic structures are preserved.