Abstract
Diabetic neuropathy is the most common complication of diabetes mellitus. Many patients with neuropathy have various forms of symptoms, including hyperalgesia and spontaneous pain. Although the mechanisms by which such neuropathic symptoms develop remain unclear, the increased spontaneous activity of dorsal root ganglion (DRG) neurons has been proposed to cause hyperalgesia in diabetes. The voltage-gated ion channels are essential for the initiation and propagation of action potentials in many excitable cells. Among them, the voltage-dependent sodium/calcium channels are highly expressed in the somata of small DRG neurons, previous workers have investigated the alteration of activities of these channels in association with pathogenesis of diabetic neuropathy. To clarify the mechanism of painful diabetic neuropathy, we examined the tetrodotoxin-resistant sodium current (TTX-R INa) and intracellular calcium concentration in isolated small DRG neurons from control and diabetic rats. We found that the TTX-R INa in diabetic DRG neurons was enhanced in amplitude and was activated at more negative potentials compared with that in control neurons, and we also found that the duration of calcium transients induced by high extracellular K+ in small DRG neurons was significantly prolonged compared with that in control neurons. These results suggest that both sodium and calcium channels play important roles in the pathogenesis of painful diabetic neuropathy. [J Physiol Sci. 2008;58 Suppl:S36]
