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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Mitochondrial immobilization mediated by syntaphilin facilitates survival of demyelinated axons
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Mitochondrial immobilization mediated by syntaphilin facilitates survival of demyelinated axons

机译：Mitochondrial immobilization mediated by syntaphilin facilitates survival of demyelinated axons

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摘要

Axonal degeneration is a primary cause of permanent neurological disability in individuals with the CNS demyelinating disease multiple sclerosis. Dysfunction of axonalmitochondria and imbalanced energy demand and supply are implicated in degeneration of chronically demyelinated axons. The purpose of this study was to define the roles of mitochondrial volume and distribution in axonal degeneration following acute CNS demyelination. We show that the axonal mitochondrial volume increase following acute demyelination of WT CNS axonsdoesnotoccur indemyelinatedaxonsdeficient insyntaphilin,an axonal molecule that immobilizes stationary mitochondria to microtubules. These findings were supported by time-lapse imaging of WT and syntaphilin-deficient axons in vitro. When demyelinated, axons deficient in syntaphilin degenerate at a significantly greater rate than WT axons, and this degeneration can be rescued by reducing axonal electrical activity with theNa~+ channelblocker flecainide. These results support theconceptthatsyntaphilin-mediatedimmobilizationofmitochondria to microtubules is required for the volume increase of axonal mitochondria following acute demyelination and protects against axonal degeneration in the CNS.

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