Department of Pathology and Laboratory Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA.
J Neurosci. 2012 Apr 4;32(14):5010-5. doi: 10.1523/JNEUROSCI.0526-12.2012.
Iron is critical in multiple aspects of CNS development, but its role in neurodevelopment--the ability of iron deficiency to alter normal development--is difficult to dissociate from the effects of anemia. We developed a novel dietary restriction model in the rat that allows us to study the effects of iron deficiency in the absence of severe anemia. Using a combination of auditory brainstem response analyses (ABR) and electron microscopy, we identified an unexpected impact of nonanemic iron deficiency on axonal diameter and neurofilament regulation in the auditory nerve. These changes are associated with altered ABR latency during development. In contrast to models of severe iron deficiency with anemia, we did not find consistent or prolonged defects in myelination. Our data demonstrate that iron deficiency in the absence of anemia disrupts normal development of the auditory nerve and results in altered conduction velocity.
铁在中枢神经系统发育的多个方面都至关重要，但铁在神经发育中的作用（即缺铁是否会改变正常发育）很难与贫血的影响区分开来。我们在大鼠中开发了一种新的饮食限制模型，使我们能够在不发生严重贫血的情况下研究缺铁的影响。我们结合听觉脑干反应分析（ABR）和电子显微镜，发现非贫血性缺铁对听神经轴突直径和神经丝调节有意外影响。这些变化与听觉脑干反应潜伏期在发育过程中的改变有关。与伴有贫血的严重缺铁模型不同，我们没有发现髓鞘形成的一致或持续缺陷。我们的数据表明，在不贫血的情况下缺铁会破坏听神经的正常发育，并导致传导速度改变。
