Iron deficiency on neuronal function
Iron deficiency on neuronal function
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DOI：
10.1007/s10534-012-9550-x
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发表时间：
2012-08-01
期刊：
影响因子：
3.5
通讯作者：
Humeres, Alexis
中科院分区：
文献类型：
--
作者：
Munoz, Pablo;Humeres, Alexis
由于铁催化活性氧形成的内在能力，它与氧化应激和神经退行性疾病有关。然而，铁缺乏（ID）也会对大脑的各种功能产生负面影响，表明铁在神经元过程中起着重要的生理作用，如髓鞘形成，突触发生，行为和突触可塑性（SP）。ID不仅会引起海马体、纹状体、杏仁核或前额叶皮质的变化，还会影响这些系统之间的相互作用。在人类和啮齿动物中，这些结构的扰动与认知缺陷有关。这些认知改变与神经可塑性的变化密切相关，神经可塑性是记忆和学习的可能细胞基质。鉴于SP受到早期ID的强烈影响，并且即使在ID已被纠正后，持久的神经学后果仍然存在，因此预防ID以及寻求有效的治疗干预以减少或逆转ID在神经系统中的长期影响是重要的。本文综述了铁缺乏对神经元功能如行为、神经传递和SP的影响。我们还讨论了我们最近的数据，铁可能的氧化作用对神经可塑性的机制。
Because of the intrinsic ability of iron to catalyze the formation of reactive oxygen species, it has been associated with oxidative stress and neurodegenerative diseases. However, iron deficiency (ID) also negatively impacts various functions of the brain, suggesting that iron plays an important physiological role in neuronal processes such as myelination, synaptogenesis, behavior and synaptic plasticity (SP). ID not only produces changes in the hippocampus, striatum, amygdale or prefrontal cortex, it also affects the interaction among these systems. In both humans and rodents, the perturbations of these structures are associated to cognitive deficits. These cognitive alterations have been well correlated with changes in neural plasticity, the possible cellular substrate of memory and learning. Given that SP is strongly affected by early ID and the lasting-neurological consequences remain even after ID has been corrected, it is important to prevent ID as well as to seek effective therapeutic interventions that reduce or reverse the long-term effects of the ID in the nervous system. This review will give an overview of the literature on the effects of iron deficit in neuronal functions such as behavior, neurotransmission and SP. We also discuss our recent data about the possible oxidative effect of iron on the mechanisms involved in neural plasticity.