Nitric oxide donors reversibly block axonal conduction: demyelinated axons are especially susceptible.

摘要: Diseases such as multiple sclerosis and Guillain-Barre syndrome are characterized not only by widespread loss of myelin from nerve fibres, but also inflammation in the central peripheral nervous systems, respectively. While demyelination alone is sufficient to block conduction thereby cause symptoms, there increasing evidence that may contribute significantly block, although mechanisms understood. Nitric oxide an important inflammatory mediator which elevated within system can be experimentally applied tissues using nitric donors. We report compounds reversible both normal demyelinated axons systems. Notably, early remyelinated particularly sensitive oxide, so at lower concentrations, including those expected sites inflammation, selectively affected. therefore propose directly symptoms via release, inhibition release open a new therapeutic avenue for demyelinating disease.