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Aerobic exercise including swimming plays a suitable role in improving somatosensory injuries. Neuropathic pain is a debilitating condition that occurs following injury or diseases of somatosensory system. In the present study, we tried to investigate the effect of exercise on myelin protein zero of sciatic nerve injured rats. Forty male rats (180–220 g) were divided into five groups (intact, sham, sham + exercise, neuropathy, and neuropathy + exercise). Right Sciatic nerve of anesthetized rats was exposed and loosely ligated (four ligations with 1 mm apart) using catgut chromic sutures to induce neuropathy. After 3 days of recovery, swimming exercise began (20 min/day/5 days a week/4 weeks). Mechanical allodynia and thermal hyperalgesia were detected using Von Frey filaments and plantar test, respectively. Sciatic nerve at the place of injury was dissected out to measure the myelin protein zero by western blot analysis. In the intact and sham groups, sciatic nerve removed at the place similar to injured group. We found that neuropathy significantly ( p  &lt; 0.05) reduced paw withdrawal mechanical and thermal thresholds and swimming exercise significantly ( p  &lt; 0.05) increased paw withdrawal mechanical and thermal thresholds compared to the neuropathy group. Moreover, we found that MPZ level significantly ( p  &lt; 0.01) decreased in neuropathy group against that in sham group, and exercise prominently ( p  &lt; 0.05) reversed MPZ level towards control level. Swimming exercise improves myelin protein zero level in neuropathic rats along with attenuating neuropathic pain. This is a promising approach in improving neuropathological disorders including Charcot-Marie-Tooth and Dejerine–Sottas disease.

somatosensory and motor research

Exercise induced myelin protein zero improvement in neuropathic pain rats Swimming exercise preserves myelin protein zero in a rat’s neuropathic pain model