Node of Ranvier remodeling in chronic psychosocial stress and anxiety

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 plastic...

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Published in:Neuropsychopharmacology (New York, N.Y.) N.Y.), 2023-09, Vol.48 (10), p.1532-1540
Main Authors: Koskinen, Maija-Kreetta, Laine, Mikaela, Abdollahzadeh, Ali, Gigliotta, Adrien, Mazzini, Giulia, Journée, Sarah, Alenius, Varpu, Trontti, Kalevi, Tohka, Jussi, Hyytiä, Petri, Sierra, Alejandra, Hovatta, Iiris
Format: Article
Language:English
Subjects:
Anxiety
Anxiety disorders
Axons
Morphology
Myelin
Nodes of Ranvier
Prefrontal cortex
Risk factors
Social interactions
Stress
Substantia grisea
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Summary: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.
ISSN:0893-133X
1740-634X
DOI:10.1038/s41386-023-01568-6