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Neuroimmunological aspects of the alterations in zinc homeostasis in the pathophysiology and treatment of depression

Published online by Cambridge University Press:  18 September 2015

Gabriel Nowak
Affiliation:
Dept. of Neurobiology Lab. of Radioligand Research, Collegium Medicum, Jagiellonian University, Kraków, Poland
Marta Kubera
Affiliation:
Dept. of Endocrinology, Institute of Pharmacology, Polish Academy of Sciences, Smêtna 12, PL 31 -343 Kraków, Poland
Michael Maes*
Affiliation:
Dept. of Psychiatry & Neuropsychology, University of Maastricht, The Netherlands
*
Department of Psychiatry and Neuropsychology, University Hospital of Maastricht, Postbus 5800, 6202 AZ Maastricht, The Netherlandscrc-mh@online.be

Summary

Zinc is a trace element which plays a fundamental role in a wide range of biochemical processes in living organisms. Zinc is an essential component of various proteins and is an important factor for physiological function of the mammalian nervous and immune systems. In the central nervous system (CNS), zinc is found at high concentrations in hippocampal neurons. These neurons possess mechanisms for zinc uptake and storage in synaptic terminals and for the stimulation of zinc release along with neurotransmitters. In the central nervous system, zinc modulates predominantly the excitatory (glutamatergic) and inhibitory (GABAergic) amino acid neurotransmission pathways. In the immune system, zinc is necessary for the physiological activity of the thymus and T-cell-dependent responses. Zinc deficiency impairs the activities of the neuroendocrine and immune systems in mammalian organisms. This paper reviews the alterations in the blood and brain zinc concentrations in relation to the neuroimmune pathophysiology and treatment of depression. Major depression is related to lowered serum zinc concentrations, which may be caused by the acute phase and the inflammatory response in that illness. Repeated administration of antidepressants selectively increases and redistributes brain zinc in the hippocampus. Since zinc is an inhibitor of the glutama-te/NMDA receptor, these data are in accordance with the glutamate hypothesis of antidepressant action.

Type
Articles
Copyright
Copyright © Scandinavian College of Neuropsychopharmacology 2000

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