title: Zn(2+): a novel ionic mediator of neural injury in brain disease.
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.
authors.affiliation: University of California, Irvine, CA 92697-4292, USA. jweiss@uci.edu
authors.forename: J H
authors.initials: JH
authors.lastname: Weiss
authors.forename: S L
authors.initials: SL
authors.lastname: Sensi
authors.forename: J Y
authors.initials: JY
authors.lastname: Koh
mesh_terms: D000818:Animals; D001927:Brain Diseases / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D006801:Humans; D019636:Neurodegenerative Diseases / Q000209:etiology / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D017729:Presynaptic Terminals / Q000378:metabolism*; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D015032:Zinc / Q000378:metabolism / Q000502:physiology*
chemical_list: D015220:Calcium Channels; D016194:Receptors, N-Methyl-D-Aspartate; D015032:Zinc