The Role Of Spinal Glial Cells And Pro-inflammatory Cytokines In Spared Nerve Injury (SNI) Model

Part OneBackground The pathophysiological mechanisms of neuropathic pain are not fully understood. Recently, more attentions have been focused on spinal glial cells which may be the key role in the generating and maintaining neuropathic pain states. Objective In the present study, we investigate the role of spinal glial cells activation in neuropathic pain in a recently developed spared nerve injury (SNI) animal model by Decosterd and Woolf. Methods In rats, a lesion was made to two of the three terminal branches of the sciatic nerve (tibial and common peroneal nerves) leaving the sural nerve intact. Continuously intrathecal administration of propentofylline, a glial modulating agent, 1 day before and 5 days after operation, was performed to disrupt spinal cord glia function. The vehicle was intrathecally administrated as control. The paw withdrawal threshold to mechanical stimulation (paw withdrawal mechaical threshold PWMT), body weight and motor function were determined pre- and post-surgery. Results It produced a prolongedmechanical allodynia in the medial and lateral part of the ipsilateral hind paw in SNI models. The treatment with propentofylline significantly prevented the development of mechanical allodynia located in either medial or lateral plantar surface. Rats in two groups showed normal motor function and body weight increase. Discuss SNI model can be applied as a useful method with little variance in searching the mechanism of neuropathic pain. These study suggest that spinal glia activation may contribute to mechanical allodynia induced by SNI.