To elucidate the role of monoamine participation in the selective regional vulnerability to ischemia, we investigated whether dopamine release into the extracellular fluid is associated with changes in the properties of the D1 and/or D2-receptors. Mongolian gerbils subjected to bilateral common carotid artery occlusion (15 min) with and without recirculation (2 hrs) served as a model for ischemia. The release of dopamine and its metabolites from the cortex and striatum has been determined in the dialysate of the extracellular fluid. Cortical and striatal membranes were used to determine the properties of D1- (inhibitory) and D2 (Stimulatory) receptors with their respective radioligands (125[1]) SCH 23982 or (3H)YM 09151-2] for binding assays. The ischemic release of dopamine was greater from the striatum (20-45pmol/l0 microliters) than that released from the cortex (O.6pmol/lO microliters). A lower affinity for D1-binding sites was observed in the striatum after ischemia only when compared to that of sham controls. Moreover, a decrease in the number of binding sites for D1-ligands was observed at the same time. No significant changes in the D2-binding properties were seen in the cortex. These findings strongly suggest that the ischemic release of dopamine from the striatum but not from the cortex is associated with early changes in the stimulatory (D2-) and inhibitory (D1-) neurotransmission.
