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

Full Abstract

OBJECTIVE: To 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. METHODS: Latent 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. RESULTS: There 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. CONCLUSIONS: Hyperglycemia 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. SIGNIFICANCE: Reduced nodal Na+ currents may partly contribute to the pathophysiology of human diabetic neuropathy.

Author information

Author/s: Misawa, Sonoko (S); Kuwabara, Satoshi (S); Kanai, Kazuaki (K); Tamura, Noriko (N); Nakata, Miho (M); Ogawara, Kazue (K); Yagui, Kazuo (K); Hattori, Takamichi (T);

Affiliation: Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.

Journal and publication information

Publication Type: Journal Article

Journal: Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology (Clin Neurophysiol), published in Netherlands. (Language: eng)

Reference: 2006-Apr; vol 117 (issue 4) : pp 815-20

Dates: Created 2006/03/20; Completed 2006/06/08; Revised 2008/09/10;

PMID: 16495151, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

Comments and Corrections

CommentIn: Clin Neurophysiol. 2006 Apr;117(4):712-3. (PMID: 16497553)

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