dithizone and Nerve-Degeneration

Zinc is present in presynaptic nerve terminals throughout the mammalian central nervous system and likely serves as an endogenous signaling substance. However, excessive exposure to extracellular zinc can damage central neurons. After transient forebrain ischemia in rats, chelatable zinc accumulated specifically in degenerating neurons in the hippocampal hilus and CA1, as well as in the cerebral cortex, thalamus, striatum, and amygdala. This accumulation preceded neurodegeneration, which could be prevented by the intraventricular injection of a zinc chelating agent. The toxic influx of zinc may be a key mechanism underlying selective neuronal death after transient global ischemic insults.

Topics: Aminoquinolines; Animals; Brain; Cell Death; Chelating Agents; Dithizone; Edetic Acid; Fluorescent Dyes; Hippocampus; Ischemic Attack, Transient; Microscopy, Fluorescence; Nerve Degeneration; Neurons; Presynaptic Terminals; Pyramidal Cells; Rats; Tosyl Compounds; Zinc