Abstract
BackgroundNeuropathic pain is a common and intractable sequel of brachial plexus injury.Materials and methodsTo investigate the underlying mechanisms, we established a unique model of neuropathic pain in rats by creating brachial plexus avulsion injury.ResultsBehavioral test of mechanical stimulation suggested that all rats developed neuropathic pain, and the pain thresholds of bilateral hind limbs significantly decreased. GFAP expression in the cervical spinal cord appeared on day 1 post-injury and increased on day 4. Ionized calcium-binding adaptor molecule 1 expression appeared on day 1 post-injury and increased until day 28. Therefore, the brachial plexus avulsion injury model can imitate the development of neuropathic pain and maintain it.ConclusionThe activation of astrocyte and microglia in the spinal cord plays a key role in the mechanism and treatment of neuropathic pain.
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