The mechanism of painful diabetic neuropathy remains unknown. Spontaneous activity in nociceptive primary afferents has been implicated in the genesis of chronic pain due to peripheral nerve injury, and diabetic axonopathy shares some histologic features with traumatic neuropathy. We hypothesized that spontaneous hyperactivity of nociceptive neurons might represent the neurophysiologic mechanism of diabetic neuropathic pain. To test this, we examined the spontaneous activity of primary afferent axons from diabetic BB/Wistar and normal Wistar rat saphenous nerves isolated from central and peripheral connections. Microfilament recordings from diabetic nerves showed a significantly higher incidence of spontaneous discharges in comparison to normal nerves. Furthermore, this spontaneous hyperactivity occurred almost exclusively in potentially nociceptive C-fibers. We conclude that in the diabetic BB/Wistar rat, spontaneous impulses are generated in potential nociceptive primary afferent neurons, and that this may represent the mechanism of chronic diabetic neuropathic pain.
|Original language||English (US)|
|Number of pages||4|
|Publication status||Published - 1985|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Internal Medicine