THE ROLE OF ZINC IN SELECTIVE NEURONAL DEATH AFTER TRANSIENT GLOBAL CEREBRAL-ISCHEMIA

Zinc is present in presynaptic nerve terminals throughout the mammalia n central nervous system and likely serves as an endogenous signaling substance. However, excessive exposure to extracellular zinc can damag e central neurons. After transient forebrain ischemia in rats, chelata ble zinc accumulated specifically in degenerating neurons in the hippo campal hilus and CA1, as well as in the cerebral cortex, thalamus, str iatum, and amygdala. This accumulation preceded neurodegeneration, whi ch could be prevented by the intraventricular injection of a zinc chel ating agent. The toxic influx of zinc may be a key mechanism underlyin g selective neuronal death after transient global ischemic insults.