ArticleProceedings of the National Academy of Sciences of the United States of America2025
Impaired AIS plasticity in ankyrin-G mutant mice alters cortical excitability and behavior.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Genomic structural equation modeling reveals the shared genetic architecture of osteosarcopenia across five musculoskeletal phenotypes.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
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Abstract
The developing brain undergoes neuroplasticity driven by learning, experience, and memory formation. The axon initial segment (AIS) is a specialized membrane domain within the proximal axon that initiates action potential. Studies have demonstrated that the AIS exhibits plasticity by altering its length and/or localization to adjust the excitability in response to neural stimuli. However, how AIS plasticity may affect brain function is unclear. The 480-kDa giant ankyrin-G protein (gAnkG) is the master organizer of AISs and nodes of Ranvier. Previously, we reported that a neurodevelopmental disorder-linked variant (Thr1861Met) in the neuron-specific domain of gAnkG causes the formation of diffused AISs in cultured ankyrin-G null neurons. Here, we generated a knock-in mouse harboring this mutation. The knock-in mice displayed impairments in motor coordination and social interaction. Neurons from these knock-in mice formed elongated AISs with no significant reduction in the accumulation of key AIS components-including ankyrin-G, β4-spectrin, voltage-gated sodium channels, and neurofascin. Crucially, unlike wild-type AISs, which shorten in response to stimulation by high K
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