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Department of Preventive Medicine and Community Health and
*
Center for Bioengineering and Department of Neuroscience, University of Texas Medical Branch, Galveston, TX 77555-1109;
NeuroBioTex, Incorporated, Galveston, TX 77550; and
**
U.S. Department of Agriculture, Agricultural Research Service Grand Forks Human Nutrition Research Center, Grand Forks, ND 58201
2To whom correspondence should be addressed.
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.
KEY WORDS: zinc brain hippocampus neurotransmission cognition
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