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郎飞结重塑在慢性心理社会应激和焦虑中的作用。

Node of Ranvier remodeling in chronic psychosocial stress and anxiety.

机构信息

SleepWell Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.

Department of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Helsinki, Finland.

出版信息

Neuropsychopharmacology. 2023 Sep;48(10):1532-1540. doi: 10.1038/s41386-023-01568-6. Epub 2023 Mar 22.

Abstract

Differential expression of myelin-related genes and changes in myelin thickness have been demonstrated in mice after chronic psychosocial stress, a risk factor for anxiety disorders. To determine whether and how stress affects structural remodeling of nodes of Ranvier, another form of myelin plasticity, we developed a 3D reconstruction analysis of node morphology in C57BL/6NCrl and DBA/2NCrl mice. We identified strain-dependent effects of chronic social defeat stress on node morphology in the medial prefrontal cortex (mPFC) gray matter, including shortening of paranodes in C57BL/6NCrl stress-resilient and shortening of node gaps in DBA/2NCrl stress-susceptible mice compared to controls. Neuronal activity has been associated with changes in myelin thickness. To investigate whether neuronal activation is a mechanism influencing also node of Ranvier morphology, we used DREADDs to repeatedly activate the ventral hippocampus-to-mPFC pathway. We found reduced anxiety-like behavior and shortened paranodes specifically in stimulated, but not in the nearby non-stimulated axons. Altogether, our data demonstrate (1) nodal remodeling of the mPFC gray matter axons after chronic stress and (2) axon-specific regulation of paranodes in response to repeated neuronal activity in an anxiety-associated pathway. Nodal remodeling may thus contribute to aberrant circuit function associated with anxiety disorders.

摘要

慢性心理社会应激可导致髓鞘相关基因表达差异和髓鞘厚度改变,这是焦虑障碍的一个风险因素。为了确定应激是否以及如何影响Ranvier 结的结构重塑,这是另一种形式的髓鞘可塑性,我们开发了 C57BL/6NCrl 和 DBA/2NCrl 小鼠中内侧前额叶皮质(mPFC)灰质中节点形态的 3D 重建分析。我们确定了慢性社交挫败应激对 C57BL/6NCrl 应激抗性和 DBA/2NCrl 应激易感小鼠 mPFC 灰质中节点形态的应变依赖性影响,包括与对照组相比,C57BL/6NCrl 应激抗性小鼠的旁突缩短和 DBA/2NCrl 应激易感小鼠的节点间隙缩短。神经元活动与髓鞘厚度变化有关。为了研究神经元激活是否是影响 Ranvier 结形态的机制,我们使用 DREADDs 反复激活腹侧海马体到 mPFC 通路。我们发现,在刺激的而不是附近未刺激的轴突中,焦虑样行为减少和旁突缩短。总之,我们的数据表明(1)慢性应激后 mPFC 灰质轴突的节段性重塑,以及(2)在与焦虑相关的通路中,神经元活动的反复作用导致轴突特异性的旁突调节。因此,节段性重塑可能导致与焦虑障碍相关的异常回路功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e691/10425340/6f0542814f99/41386_2023_1568_Fig1_HTML.jpg

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