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Trends Pharmacol Sci. 2000 Oct;21(10):395-401.

Zn(2+): a novel ionic mediator of neural injury in brain disease.

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1
University of California, Irvine, CA 92697-4292, USA. jweiss@uci.edu

Erratum in

  • Trends Pharmacol Sci 2000 Dec;21(12):496.

Abstract

Zn(2+) is the second most prevalent trace element in the body and is present in particularly large concentrations in the mammalian brain. Although Zn(2+) is a cofactor for many enzymes in all tissues, a unique feature of brain Zn(2+) is its vesicular localization in presynaptic terminals, where its release is dependent on neural activity. Although the physiological significance of synaptic Zn(2+) release is little understood, it probably plays a modulatory role in synaptic transmission. Furthermore, several lines of evidence support the idea that, upon excessive synaptic Zn(2+) release, its accumulation in postsynaptic neurons contributes to the selective neuronal loss that is associated with certain acute conditions, including epilepsy and transient global ischaemia. More speculatively, Zn(2+) dis-homeostasis might also contribute to some degenerative conditions, including Alzheimer's disease. Further elucidation of the pathological actions of Zn(2+) in the brain should result in new therapeutic approaches to these conditions.

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PMID:
11050320
[Indexed for MEDLINE]

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