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Objective Following the input of peripheral nociceptive information, some proinflammatory cytokines from microglia, such as TNF-α, will be released, and further produce and maintain the hyperalgesia and allodynia.However, its mechanism is not yet clear.NR1 is a necessary subunit of NMDAR, and its well known that phosphorylation of NR1 (p-NR1) can upregulate the plasticity of synaptic transmission, which is the essentials of hyperalgesia and allodynia.In consequence, the present study was undertaken to determine whether TNF-α can mediate hyperalgesia and allodynia by upregulating spinal p-NR1 expression in rats.Methods The paw withdrawal latency (PWL) test for assessing hyperalgesia / allodynia and Western blot for measuring p-NR1 were implemented in the models of CFA-induced peripheral inflammation hyperalgesia or in the rats of TNF-α agonist intrathecally administration.Results (1) Thermalgia responses and spinal p-NR1 expression will be upregulated in the models of CFA-induced peripheral inflammation pain, which can be alleviated by TNF-α antagonist; (2) Intrathecal administration of TNF receptor (TNFR1) agonist will induce the development of hyperalgesia / allodynia, and enhance the expression of p-NR1 in normal rats, which also can be prevented by TNF-α antagonist.Conclusion TNF-α mediates hyperalgesia and allodynia by upregulating p-NR1 expression in spinal cord in rats.