Journal
BRAIN RESEARCH
Volume 1715, Issue -, Pages 57-65Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2019.03.016
Keywords
Neuropathic pain; Alpha7 acetylcholine receptor; Dynorphin A
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Funding
- National Natural Science Foundation of China (NSFC) [81270414, 2017GXL-008]
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Dynorphin A is increased in neuropathic pain models. Activation of alpha 7 n acetylcholine receptor (nAchR) reduces inflammation and pain. Whether activation of alpha 7 nAchR affects dynorphin A release is unknown. The experiments evaluated the proinflammatory effect of dynorphin A in the spinal nerve ligation-induced neuropathic pain models and the effect of alpha 7 nAchR activation on the dynorphin A content. a alpha 7 nAchR agonist, PHA-543613 and its antagonist, methyllycaconitine citrate were used and dynorphin A content was measured after spinal nerve ligation and in microglia cultures to test the analgesic mechanisms of alpha 7 nAchR activation. The results showed that dynorphin A content peaked 3 to 7 days after nerve injury, and dynorphin A anti-serum intrathecal injection decreased IL-beta and TNF-alpha content a week after nerve injury. Activation of alpha 7 nAchR by PHA-543613 alleviated neuropathic pain behaviors and decreased dynorphin A concentration in the ipsilateral spinal cords. Also, PHA-543613 decreased dynorphin A release from the microglia cultures to LPS stimulation by activation of alpha 7 nAchR. Our results suggest that dynorphin A contribute to the development and maintenance of neuropathic pain and that decreasing dynorphin A content by activation of alpha 7 AchR of microglia is a potential therapeutic target for treating neuropathic pain.
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