Zinc: development and function of the brain

Zn is essential for synthesis of nucleic acids and protein. In rodents Zn d eficiency in early gestation causes teratology and death. Later it impairs neuronal division and maturation. Behavioral sequellae in offspring persist into adulthood. Acute deficiency also impairs behavior. Oxidation of metal lothionein by GSSG releases Zn to specific ligands. Zn-ATP facilitates acti vity of pyridoxal-kinase and flavokinase for synthesis of PLP and FAD, resp ectively the coenzymes for biogenic-amine synthesis and MAO metabolism. Zn containing vesicles in presynaptic axon terminals of a special class of glu taminergic neurons release Zn into the synaptic cleft during neurotransmiss ion. Zn modulates postsynaptic N-methyl-D-aspartate (NMDA) excitatory recep tors for glutamate. Zn deficiency decreases the number of post-synaptic NMD A specific glutamate mediated calcium channels. In humans Zn deficiency imp airs neuropsychological functions. Severe deficiency causes ataxia and abno rmal mentation. Mild deficiency impairs neuromotor coordination and cogniti ve functions such visual memory and reasoning. Maternal Zn status during pr egnancy affects outcomes including fetal growth, head-size, neonatal perfor mance, and later behaviors of infants. Limited data suggest Zn nutriture af fects neuronal survival in elderly.