Effects of cerebral ischemia on dopamine receptors in the gerbil striatum

Dopamine D1 and D2 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. [3H]SCH23390 ([N-methyl-3H]R[+]-8-chloro-2, 3,4,5-tetrahydro-3-methyl-5-phenyl-7-ol-benzazepine), [3H]nemonapride and [3H]mazindol were used as markers of dopamine D1 receptors, D2 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, [3H]nemonapride and [3H]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 [3H]SCH23390, [3H]nemonapride and [3H]mazindol binding after ischemia. Thus, cerebral ischemia that was associated with cell loss in the striatum resulted in a selective reduction of dopamine D1 receptors and not D2 receptors. No changes in dopamine D1 or D2 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.