Zinc, nervous system and aging.

Abstract

required for quick inactivation of hormones or neurotransmitters justify its involvement also in actual performance of the nervous system. Thus, zinc-dependent dopamine-beta-hydrolase and phenylethanolamine-N-methyl transferase are required to convert dopamine to norepinephrine and this later into epinephrine respectively; glutamate dehydrogenase is involved in the metabolism of glutamic acid. Zinc acts as a cofactor in the metalloenzyme enkephalinase, thus contributing to the degradation of enkephalin and, possibly, also of cholecystokinin-octapeptide. Zinc may interfere with the binding to receptor of gamma-aminobutyric acid, of acetylcholine and of benzodiazepines. Finally, many of the so-called metaboreceptors are also zinc-dependent. The ionic zinc, which is the fraction of tissue zinc that can be demonstrated histochemically, appears to be intimately associated with the secretory-signaling functions of certain neurones. The highest levels of the ion occur in the hippocampal mossy fiber (MF) pathway. This system forms a dense plexus of terminals on apical dendrites of CA3 pyramidal neurons and is involved in the modulation of processes related to spatial learning and memory. The synaptic terminals of the mossy fibers are uniquely rich in Zn 2+ , which is actively taken up and stored in a pool of synaptic vesicles. Stimulation of the MF can induce Zn release, suggesting that the ion may affect neurotransmission. It has been observed that a reduction of the hippocampal Zn levels, obtained with chelating agents, can induce in adult animals spatial memory deficits and reduced learning ability. In humans some evidence exists of impaired concentration, jitteriness, lethargy, depression and mood lability, as well as disturbed taste and smell perception in individuals suffering from suspected zinc deficiency. From a clinical point of view many are the neuropathologies associated with alterations of zinc status. Zinc has been found reduced in schizophrenia, mental depression, dyslexia, multiple sclerosis, Guillain