Abstract
A link between copper metabolism and endogenous opiates or their receptors and peptides has been suggested by the work from several laboratories (1–4). In humans, Kolb and Sadee proposed a relationship between copper metabolism, endorphins and schizophrenia (5). Early work in animals have shown that central nervous system disorders such as ataxia, motor incoordination and brain and spinal cord degeneration occur in experimental copper deficiency (6–9). Though not specifically mentioned, it is possible that some alteration in opiates (besides alteration in neurotransmitters) could have occurred. A critical role of copper in the brain development has been suggested by Zimmerman et al. (10). O’Dell et al. have reported decreased concentration of dopamine and norepinephrine in brain in experimental copper deficiency (11–13) and that repletion with copper restores the level of norepinephrine (13).
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Bhathena, S.J., Recant, L. (1987). Peptides and Opiates in Copper Deficiency. In: Sorenson, J.R.J. (eds) Biology of Copper Complexes. Experimental Biology and Medicine, vol 16. Humana Press. https://doi.org/10.1007/978-1-4612-4584-1_24
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DOI: https://doi.org/10.1007/978-1-4612-4584-1_24
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