title: History of zinc as related to brain function.
abstract: Zinc (Zn) is essential for synthesis of coenzymes that mediate biogenic-amine synthesis and metabolism. Zn from vesicles in presynaptic terminals of certain glutaminergic neurons modulates postsynaptic N-methyl-D-aspartate (NMDA) receptors for glutamate. Large amounts of Zn released from vesicles by seizures or ischemia can kill postsynaptic neurons. Acute Zn deficiency impairs brain function of experimental animals and humans. Zn deficiency in experimental animals during early brain development causes malformations, whereas deficiency later in brain development causes microscopic abnormalities and impairs subsequent function. A limited number of studies suggest that similar phenomena can occur in humans.
authors.affiliation: Department of Preventive Medicine and Community Health, University of Texas Medical Branch, Galveston 77555-1109, USA.
authors.forename: H H
authors.initials: HH
authors.lastname: Sandstead
authors.forename: C J
authors.initials: CJ
authors.lastname: Frederickson
authors.forename: J G
authors.initials: JG
authors.lastname: Penland
mesh_terms: D000818:Animals; D001921:Brain / Q000002:abnormalities / Q000254:growth & development / Q000502:physiology; D003071:Cognition / Q000187:drug effects; D005260:Female; D049673:History, 20th Century; D006801:Humans; D008297:Male; D015032:Zinc / Q000172:deficiency / Q000266:history* / Q000502:physiology
chemical_list: D015032:Zinc