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Spinal cord injury (SCI) induces incapacitating neuropathic pain in the form of allodynia-a painful response to normally non-noxious stimuli. Unfortunately, the underlying mechanisms of these sensory changes are not well understood, and effective treatments for allodynia have proven elusive. We examined whether physical exercise can improve sensory function after experimental SCI by promoting neurotrophin expression in the spinal cord and periphery, which modulates synaptic transmission and function. Female rats with moderate spinal cord contusion participated in treadmill training, swim training, stand training or were untrained. Exercise training began 4 days post surgery, lasted 20-25 min per day, 5 days a week for 7 weeks. Allodynia, as measured using von Frey hairs of different bending forces to the plantar hind paw, developed in the untrained group 3 weeks after SCI. Treadmill training ameliorated allodynia and restored normal sensation by 5 weeks. Swim training had a transient beneficial effect, but allodynia returned by 7 weeks. Stand training had no effect. Resolution of allodynia after treadmill training was associated with normal mRNA levels of brain-derived neurotrophic factor (BDNF) in both the lumbar spinal cord and soleus muscle. No other exercise paradigm restored BDNF centrally and peripherally. Greater recovery from allodynia correlated significantly with the degree of normalization of central and peripheral BDNF levels. These findings suggest that rhythmic, weight-bearing exercise may be an effective intervention to counter SCI-induced allodynia.

Three exercise paradigms differentially improve sensory recovery after spinal cord contusion in rats