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 ge rbil striatum and frontal cortex 1 h to 7 days after 10 min of cerebra l ischemia caused by occlusion of the bilateral common carotid arterie s. [H-3]SCH23390 ,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]n emonapride and [H-3]mazindol binding was mostly unaffected in this reg ion which was the most vulnerable to ischemia. The frontal cortex, whe re ischemic neuronal damage was mild, also showed no significant chang es in [H-3]SCH23390, [H-3]nemonapride and [H-3]mazindol binding after ischemia. Thus, cerebral ischemia that was associated with cell loss i n the striatum resulted in a selective reduction of dopamine D-1 recep tors and not D-2 receptors. No changes in dopamine D-1 or D-2 receptor s were observed in frontal cortex. If massive dopamine release occurs with cerebral ischemia, it is not reflected by modification in the num ber of uptake sites located on dopamine terminals.