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American Journal of Clinical Nutrition, Vol 50, 607-617, Copyright © 1989 by The American Society for Nutrition
1 From the Department of Pharmacology, Faculty of Medicine and Rappaport Family Research Institute, Technion Medical School, Haifa, Israel, and the Psychopharmacology Laboratory, Department of Psychology, Bar-Ilan University, Ramat-Gan, Israel
An animal model of nutritional iron deficiency (ID) is described that demonstrates a reduction of brain nonheme iron. The most prominent feature of ID is the significant and selective diminution of central dopamine neurotransmission resulting from the decreased number of dopamine D2 receptors in the caudate nucleus, nucleus accumbens, pituitary, and in all probability the frontal cortex. The consequences of diminished dopaminergic neurotransmission is a modification of dopamine-dependent behaviors and biochemical reactions, the most important of which is the reduction in learning processes. The role of iron in maintaining the homeostasis of normally functioning dopamine neurons and their involvement in cognitive processes cannot be excluded. An interference with iron metabolism at an early age can result in irreversible damage to developing dopamine neurons, with consequences that may manifest themselves in adult life.
Key Words: Iron deficiency • neurotransmitters • dopamine receptor • opiate peptides • learning
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