History of zinc as related to brain function

Zinc (Zn) is essential for synthesis of coenzymes that mediate biogenic-ami ne synthesis and metabolism. Zn from vesicles in presynaptic terminals of c ertain glutaminergic neurons modulates postsynaptic N-methyl-D-aspartate (N MDA) receptors for glutamate. Large amounts of Zn released from vesicles by seizures or ischemia can kill postsynaptic neurons. Acute Zn deficiency im pairs brain function of experimental animals and humans. Zn deficiency in e xperimental animals during early brain development causes malformations, wh ereas deficiency later in brain development causes microscopic abnormalitie s and impairs subsequent function. A limited number of studies suggest that similar phenomena can occur in humans.