• Clin Neurophysiol · Apr 2006

    Nodal persistent Na+ currents in human diabetic nerves estimated by the technique of latent addition.

    • Sonoko Misawa, Satoshi Kuwabara, Kazuaki Kanai, Noriko Tamura, Miho Nakata, Kazue Ogawara, Kazuo Yagui, and Takamichi Hattori.
    • Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
    • Clin Neurophysiol. 2006 Apr 1; 117 (4): 815-20.

    ObjectiveTo investigate the effects of hyperglycemia on persistent Na+ currents in human diabetic nerves, eliminating the factors of passive membrane properties as a factor. Previous studies show that strength-duration time constant of a nerve is shortened under hyperglycemia, suggesting reduced axonal persistent Na+ currents. However, the time constant is also affected by changes in passive membrane properties. Latent addition using computerized threshold tracking is a new method that can separately evaluate Na+ currents and passive membrane properties.MethodsLatent addition was used to estimate nodal Na+ currents in median motor axons of 83 diabetic patients. Brief hyperpolarizing conditioning current pulses were delivered, and threshold changes at the conditioning-test interval of 0.2 ms were measured as an indicator of nodal persistent Na+ currents. Seventeen patients were examined before and after insulin treatment.ResultsThere was an inverse linear relationship between hemoglobin A1c levels and threshold changes at 0.2 ms (P=0.02); the higher hemoglobin A1c levels were associated with smaller threshold changes. After insulin treatment, there was a significant improvement in nerve conduction velocities associated with greater threshold changes at 0.2 ms (P=0.03), suggesting an increase in persistent Na+ currents. The fast component of latent addition, an indicator of passive membrane properties, was not affected by the state of glycemic control.ConclusionsHyperglycemia could suppress nodal persistent Na+ currents, presumably because of reduced trans-axonal Na+ gradient or impaired Na+ channels, and this can be rapidly restored by glycemic control.SignificanceReduced nodal Na+ currents may partly contribute to the pathophysiology of human diabetic neuropathy.

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