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Effects of Cerebral Ischemia on Regional Dopamine Release and D 1 and D 2 Receptors
Author(s) -
Chang C. J.,
Ishii H.,
Yamamoto H.,
Yamamoto T.,
Spatz M.
Publication year - 1993
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.1471-4159.1993.tb03311.x
Subject(s) - striatum , microdialysis , dopamine receptor d2 , medicine , dopamine , ischemia , endocrinology , dopaminergic , receptor , cerebral cortex , chemistry , cortex (anatomy) , brain ischemia , biology , neuroscience
To expand on the nature of regional cerebral vulnerability to ischemia, the release of dopamine (DA) and dopaminergic (D 1 and D 2 ) receptors were investigated in Mongolian gerbils subjected to bilateral carotid artery occlusion (15 min) alone or with reflow (1–2 h). Extracellular cortical and striatal content of DA and its metabolites was measured by microdialysis using HPLC with electrochemical detection. The kinetic properties of D 1 and/or D 2 receptor binding sites were determined in cortical and striatal membranes with the use of radiolabeled ligands ( 125 I‐SCH23982 and [ 3 H]YM‐09151‐2, respectively). The ischemic release of DA from the striatum was greater (400‐fold over preischemic level) than that from the cortex (12‐fold over preischemic content). The affinity for the D 1 ‐receptor ligand was lower ( K D = 1.248 ± 0.047 n M ) after ischemia than that for sham controls ( K D = 0.928 ± 0.032 n M, p < 0.001). The number of binding sites for D 2 receptors decreased in striatum ( B max = 428 ± 18.4 fmol/mg of protein) after ischemia compared with sham controls ( B max = 510 ± 25.2 fmol/mg of protein, p < 0.05). D 1 or D 2 binding sites were not changed either in the ischemic cortex or postischemic striatum and cortex. The findings strongly suggest that the ischemic release of DA from striatum is associated with early transient changes in D 1 ‐ and D 2 ‐mediated DA neurotransmission.