The cortical and striatal release of biogenic amines induced by ischemia has been evaluated in dialysates of extracellular fluid. Mongolian gerbils subjected to bilateral common carotid artery occlusion for 15 minutes with a reflow up to 2 hours served as a model for transient ischemia of brain. These studies are still incomplete, but the results indicate that ischemia of short duration causes a marked release of dopamine and serotnin (5-HT) f rom both structures. The level of the released amines was higher in the striatum than in the cortex. Both metabolites of dopamine and 5-HT decreased during ischemia and increased in reflow. The findings support the idea that the selective vulnerability to ischemia may at least be in part related to ischemic disturbances of biogenic neurotransmitters.