Language
English
Publication Date
12-30-2024
Journal
Nature Communications
DOI
10.1038/s41467-024-55209-7
PMID
39738113
PMCID
PMC11686269
PubMedCentral® Posted Date
12-30-2024
PubMedCentral® Full Text Version
Post-print
Abstract
The bipolar disorder (BD) risk gene ANK3 encodes the scaffolding protein AnkyrinG (AnkG). In neurons, AnkG regulates polarity and ion channel clustering at axon initial segments and nodes of Ranvier. Disruption of neuronal AnkG causes BD-like phenotypes in mice. During development, AnkG is also expressed at comparable levels in oligodendrocytes and facilitates the efficient assembly of paranodal junctions. However, the physiological roles of glial AnkG in the mature nervous system, and its contributions to BD-like phenotypes, remain unexplored. Here, we show that oligodendroglia-specific AnkG conditional knockout results in destabilization of axoglial interactions in aged but not young adult mice. In addition, these mice exhibit significant histological, electrophysiological, and behavioral pathophysiologies. Unbiased translatomic profiling reveals potential compensatory machineries. These results highlight the functions of glial AnkG in maintaining proper axoglial interactions throughout aging and suggest a contribution of glial AnkG to neuropsychiatric disorders.
Keywords
Animals, Oligodendroglia, Mice, Knockout, Mice, Ankyrins, Aging, Bipolar Disorder, Axons, Male, Neuroglia, Mice, Inbred C57BL, Female, Behavior, Animal, Neurons, Oligodendrocyte, Molecular neuroscience
Published Open-Access
yes
Recommended Citation
Ding, Xiaoyun; Wu, Yu; Vainshtein, Anna; et al., "Age-Dependent Regulation of Axoglial Interactions and Behavior by Oligodendrocyte AnkyrinG" (2024). Faculty and Staff Publications. 3961.
https://digitalcommons.library.tmc.edu/baylor_docs/3961