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Recent evidence suggests that large amounts of releasable zinc are present in central synaptic vesicles, and that substantial (several hundred microM) transient elevations in extracellular zinc may accompany intense neuronal excitation. Brief pulse exposure of cortical cell cultures to similar concentrations of zinc resulted in widespread dose-dependent neuronal injury; exposure to higher concentrations resulted in the addition of glial injury. The results suggest that zinc should be included on the growing list of endogenous central neurotoxins which may be involved in the pathogenesis of CNS cell loss in a variety of disease states.
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Yokoyama et al. (1986) studied this question.
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