ArticleNature communications2025
Hypomyelination in autism-associated neuroligin-3 mutant mice impairs parvalbumin interneuron excitability, gamma oscillations, and sensory discrimination.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Developmental Deficiency of Oligodendrocytes and Myelination in the Central Nervous System of the Fetal Alcohol Syndrome Mouse Model.CNS neuroscience & therapeutics · 2026Article
- Myelin dysfunction in autism spectrum disorder: insights into core symptoms and mechanisms of brain development.Molecular psychiatry · 2026Review
- Mesenchymal stem/stromal cell-based therapies for autism spectrum disorder: emerging evidence and clinical prospects.Journal of translational medicine · 2026Review
- Light-based 40 Hz sensory therapy for brain disorders: physiological basis, therapeutic mechanisms, and future prospects.Frontiers in medicine · 2026Review
- Rethinking parvalbumin: From passive marker to active modulator of hippocampal circuits.IBRO neuroscience reports · 2025Article
- Parvalbumin interneurons: the dark and bright sides of a key playmaker of neural circuits and behavior.Frontiers in cellular neuroscience · 2025Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Whether and how myelin plasticity, an emerging new form of brain plasticity, is involved in autism spectrum disorder (ASD) remains unknown. Here, we identify deficits in oligodendrocyte (OL) generation and myelination in the barrel cortex (BC) of the male NL3-R451C-KI mouse model of ASD. These mice also show impaired texture recognition, disrupted gamma neuronal oscillations, and reduced excitability and myelination level in the BC-PV interneuron. These abnormalities can be rescued by a promyelinating strategy and are recapitulated by genetic blockade of myelination in Myrf-cKO mice. Furthermore, OL progenitor-specific conditional NL3 knockout mice show similar deficits in BC-PV interneuron myelination and excitability, as well as neuronal oscillation and texture recognition, closely resembling the NL3-R451C-KI phenotype. Collectively, these results demonstrate that NL3 mutations commonly cause hypomyelination and reduced excitability in BC-PV interneurons, disrupting neuronal oscillation and contributing to ASD-like sensory dysfunction. Our finding reveals a mechanism underlying ASD and highlights OLs/myelin as potential therapeutic targets for ASD.
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