神经发育障碍中突触可塑性缺陷中睡眠与突触翻译的交集。

IF 1.7 3区 生物学 Q4 PHYSIOLOGY Journal of Comparative Physiology B-Biochemical Systems and Environmental Physiology Pub Date : 2024-06-01 Epub Date: 2024-02-24 DOI:10.1007/s00360-023-01531-3
Rochelle L Coulson, Philippe Mourrain, Gordon X Wang
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引用次数: 0

摘要

越来越多的证据表明,睡眠失调是导致神经发育障碍患者出现突触和行为缺陷的根本原因,而不仅仅是一种影响。在分子水平上,突触蛋白质组失调是神经发育障碍的一个共同特征,但这些分子和行为表型之间的关联机制仍是一个有待研究的领域。eIF2α 在根据突触条件的变化改变局部蛋白质组方面的作用已经出现。在这里,我们讨论了在描述局部突触翻译和睡眠的交叉点方面的最新进展,并提出了神经发育障碍中突触可塑性缺陷发展过程中失调的互惠机制。
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The intersection of sleep and synaptic translation in synaptic plasticity deficits in neurodevelopmental disorders.

Individuals with neurodevelopmental disorders experience persistent sleep deficits, and there is increasing evidence that sleep dysregulation is an underlying cause, rather than merely an effect, of the synaptic and behavioral defects observed in these disorders. At the molecular level, dysregulation of the synaptic proteome is a common feature of neurodevelopmental disorders, though the mechanism connecting these molecular and behavioral phenotypes is an ongoing area of investigation. A role for eIF2α in shifting the local proteome in response to changes in the conditions at the synapse has emerged. Here, we discuss recent progress in characterizing the intersection of local synaptic translation and sleep and propose a reciprocal mechanism of dysregulation in the development of synaptic plasticity defects in neurodevelopmental disorders.

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来源期刊
CiteScore
3.90
自引率
0.00%
发文量
51
审稿时长
3.5 months
期刊介绍: The Journal of Comparative Physiology B publishes peer-reviewed original articles and reviews on the comparative physiology of invertebrate and vertebrate animals. Special emphasis is placed on integrative studies that elucidate mechanisms at the whole-animal, organ, tissue, cellular and/or molecular levels. Review papers report on the current state of knowledge in an area of comparative physiology, and directions in which future research is needed.
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