The Effects of Two-Week Swimming Training on Neuropathic Pain Induced by Chronic Constriction Injury and the Expression of GAD65 in Adult Male Rats

Unknown mechanisms are involved in neuropathic pain. Among the non-pharmacological treatments, it seems that physical activity improves neuropathic pain. However, the possible reasons for the effectiveness of regular physical activity on neuropathic pain are unknown. Therefore, the present study was performed to determine the effects of two-week swimming training on the expression of GAD65 enzyme and P2X3 receptor in Chronic Constriction Injury (CCI) of the sciatic nerve.
40Wistar adult rats were divided into five groups randomly: 1) CCI neuropathic pain with swimming training (CCIST2); 2) CCI neuropathic pain without swimming training (CCI); 3) No CCI neuropathic pain with swimming training (ST2); No CCI neuropathic pain without swimming training (control group); 5) CCI sham surgery (Sham CCI). CCI and CCIST2 groups underwent peripheral nerve injury by four loose ligatures around sciatic nerve. Swimming program included two weeks with five sessions per week, and 30-60 min per session. The protein expressions of GAD65 enzyme and P2X3 receptor were evaluated by western blotting technique.
CCI surgery decreased the expression of GAD65, but two weeks swimming training increased expression of GAD65 comparing to CCI and Sham CCI groups (P≤0.001), but P2X3 receptor expression were not significantly different among groups in lumbar segment of rats (P>0.05).
Totally, our findings showed that two-week swimming training improves neuropathic pain possibly through maintenance of inhibitory neurons and subsequently increased GAD65, which converts glutamate excitatory neurotransmitter to GABA inhibitory neurotransmitter.