Technical 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. Knowledge of the relationship between zinc nutriture and brain development and function has come from research in several disciplines, including neurochemistry, neuroanatomy, biology, physiology and psychology. Interestingly, many advances occurred in parallel with limited cross-disciplinary communication. This review of historical and recent research attempts to "bridge the gap" and provide a coherent story about this important and still evolving relationship.