Burchiel K J, Russell L C, Lee R P, Sima A A
Diabetes. 1985 Nov;34(11):1210-3. doi: 10.2337/diab.34.11.1210.
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.
疼痛性糖尿病神经病变的机制尚不清楚。伤害性初级传入神经的自发活动与外周神经损伤所致慢性疼痛的发生有关，并且糖尿病性轴索性神经病与创伤性神经病具有一些组织学特征。我们推测伤害性神经元的自发活动增强可能是糖尿病性神经病变性疼痛的神经生理机制。为了验证这一点，我们检测了从糖尿病BB/Wistar大鼠和正常Wistar大鼠隐神经分离出的、与中枢和外周联系切断的初级传入轴突的自发活动。与正常神经相比，糖尿病神经的微丝记录显示自发放电的发生率显著更高。此外，这种自发活动增强几乎仅发生在潜在的伤害性C纤维中。我们得出结论，在糖尿病BB/Wistar大鼠中，潜在的伤害性初级传入神经元会产生自发冲动，这可能是慢性糖尿病性神经病变性疼痛的机制。
