SleepWell Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Department of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Neuropsychopharmacology. 2023 Sep;48(10):1532-1540. doi: 10.1038/s41386-023-01568-6. Epub 2023 Mar 22.
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.
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。