Effects of cerebral ischemia on dopamine receptors in the gerbil striatum

Dopamine D-1 and D-2 receptors and uptake sites were studied in the gerbil striatum and frontal cortex 1 h to 7 days after 10 min of cerebral ischemia caused by occlusion of the bilateral common carotid arteries. [H-3]SCH23390 ([N-methyl-H-3]R[+]-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-7-ol-benzazepine), [H-3]nemonapride and [H-3]mazindol were used as markers of dopamine D-1 receptors, D-2 receptors and uptake sites, respectively. A significant reduction in [3H]SCH23390 binding was found in the striatum from 48 h after ischemia. In contrast, during the recirculation periods, [H-3]nemonapride and [H-3]mazindol binding was mostly unaffected in this region which was the most vulnerable to ischemia. The frontal cortex, where ischemic neuronal damage was mild, also showed no significant changes in [H-3]SCH23390, [H-3]nemonapride and [H-3]mazindol binding after ischemia. Thus, cerebral ischemia that was associated with cell loss in the striatum resulted in a selective reduction of dopamine D-1 receptors and not D-2 receptors. No changes in dopamine D-1 or D-2 receptors were observed in frontal cortex. If massive dopamine release occurs with cerebral ischemia, it is not reflected by modification in the number of uptake sites located on dopamine terminals.