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Nodal gap substance in diabetic nerve.

K N Seneviratne, A Weerasuriya

    Journal of Neurology, Neurosurgery, and Psychiatry
    |May 1, 1974
    PubMed
    Summary

    Diabetic nerves show increased permeability in the paranodal gap substance, impairing nerve function. This study reveals reduced potassium binding in the nodal gap substance of diabetic nerves, contributing to conduction block.

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    Area of Science:

    • Neuroscience
    • Diabetic Neuropathy Research
    • Peripheral Nerve Physiology

    Background:

    • Anoxia and potassium chloride (KC1) induce peripheral nerve inactivation via depolarization conduction block.
    • The paranodal gap substance acts as a diffusion barrier in healthy peripheral nerves.

    Purpose of the Study:

    • To investigate the role of the paranodal gap substance in healthy versus diabetic peripheral nerves.
    • To understand the impact of diabetes on nerve permeability and ion binding.

    Main Methods:

    • Comparative analysis of isolated sciatic nerves from healthy and alloxan-diabetic rats.
    • Investigation of inactivation patterns using anoxia and KC1.
    • Assessment of K' binding capacity in myelinated nerves.

    Main Results:

    • Diabetic nerves exhibit significantly increased permeability of the paranodal gap substance.
    • A marked reduction in K' binding capacity was observed in the nodal gap substance of diabetic nerves (both human and rat models).

    Conclusions:

    • The increased permeability of the paranodal gap substance in diabetic nerves contributes to impaired nerve function.
    • Reduced K' binding capacity in the nodal gap substance is a key feature of diabetic neuropathy, potentially leading to conduction deficits.

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