Background & Aims : Axonal transport is a vital process in nervous system that protects axons and nerve terminals through supplying proteins, lipids and mitochondria and clearing folded proteins to avoid toxicity. Recently it is reported that impairment of motor proteins involved in axonal transport-like dynactin is a common factor in several neurodegenerative disorders such as Amyotrophic Lateral Sclerosis (ALS). However, no study was found to investigate the abnormalities in axonal transport due to decreased physical activity and neuropathic pain.

  Materials & Methods : Ten adult male Wistar rats in the weight range of 250±30 gr were randomly divided into two groups including healthy control (C) (N=5), ligation group (SNL) (N=5). Over the six weeks, neuropathic pain behavior tests were conducted continually on the groups. In the end of the sixth weeks, change of dynactin gene expression in sciatic nerve measured with real time technique and calculated using the 2^-ΔΔCT method.

  Results : After 6 weeks, neuropathic pain behavior tests showed that pain threshold of thermal hyperalgesia and mechanical allodynia in the SNL group was significantly lower than the control group (p = 0.000). In addition, dynactin gene expression in sciatic nerve ligation group compared to controls decreased significantly (p = 0.001).

  Conclusion : It seems that neuropathic pain and decreased physical activity is associated with decreased dynactin gene expression in sciatic nerve fiber. According to the physiologic functions of dynactin in neurons, this condition may cause functional disorders in the neural and muscular systems.

  SOURCE: URMIA MED J 2015: 26(2): 120 ISSN: 1027-3727