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早期缺铁引起的轻微脑损伤:多巴胺能神经传递的改变

Minimal brain damage induced by early iron deficiency: modified dopaminergic neurotransmission.

作者信息

Youdim M B, Ben-Shachar D

出版信息

Isr J Med Sci. 1987 Jan-Feb;23(1-2):19-25.

PMID:3032848
Abstract

The reports that iron-deficiency anemia in human subjects induces behavioral changes was investigated in rats made nutritionally iron-deficient. The most prominent features of these animals were: the unchanged metabolism of the neurotransmitters noradrenaline, dopamine and serotonin, profound reduction of brain nonheme iron, the selective diminution of dopamine D2 receptor number (measured by Bmax), modification of dopamine-dependent behaviors and reduction of learning processes. The induction of these changes and their recovery with iron supplementation are age- and time-dependent phenomena. In newborn rats, however, the consequences of iron deficiency are irreversible, even after long-term iron supplementation. The results point to the profound effect iron metabolism can have on the long-term development and function of dopaminergic neurotransmission. These findings may not be totally unexpected, since iron distribution in the brain is highly localized in dopaminergic-peptidergic regions, such as the globus pallidus, substantia nigra, red nucleus, thalamus, caudate nucleus and nucleus accumbens. In some regions its concentration is higher than that found in the liver, the site of iron metabolism.

摘要

在造成营养性缺铁的大鼠中,对人体缺铁性贫血会引起行为变化的报告进行了研究。这些动物最显著的特征是:神经递质去甲肾上腺素、多巴胺和血清素的代谢未改变,脑非血红素铁显著减少,多巴胺D2受体数量选择性减少(通过Bmax测量),多巴胺依赖行为的改变以及学习过程的减少。这些变化的诱导及其通过补充铁的恢复是年龄和时间依赖性现象。然而,在新生大鼠中,即使长期补充铁,缺铁的后果也是不可逆的。结果表明铁代谢对多巴胺能神经传递的长期发育和功能可能有深远影响。这些发现可能并非完全出乎意料,因为大脑中铁的分布高度集中在多巴胺能 - 肽能区域,如苍白球、黑质、红核、丘脑、尾状核和伏隔核。在某些区域其浓度高于铁代谢部位肝脏中的浓度

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