Article Publish Status: FREE
Abstract Title:

Electroacupuncture Attenuates CFA-Induced Inflammatory Pain by Regulating CaMKII.

Abstract Source:

Neural Plast. 2020 ;2020:8861994. Epub 2020 Dec 31. PMID: 33488694

Abstract Author(s):

Yixiao Gu, Shuangdong Chen, Yunchang Mo, Yingying Tu, Na Chen, Xiaoyong Zhao, Shan Li, Qimin Yu, Qinxue Dai, Junlu Wang

Article Affiliation:

Yixiao Gu


Ca/calmodulin-dependent protein kinase II (CaMKII) is a multifunctional serine/threonine kinase that is ubiquitously distributed in the central and peripheral nervous systems. Moreover, its phosphorylated protein (P-CaMKII) is involved in memory, mood, and pain regulation in the anterior cingulate cortex (ACC). Electroacupuncture (EA) is a traditional Chinese therapeutic technique that can effectively treat chronic inflammatory pain. However, the CaMKII-GluA1 role in EA analgesia in the ACC remains unclear. This study investigated the role of P-CaMKII and P-GluA1 in a mouse model of inflammatory pain induced by complete Freund's adjuvant (CFA). There were increased P-CaMKII and P-GluA1 levels in the ACC. We found that intracerebroventricular injection of KN93, a CaMKII inhibitor, as well as EA stimulation, attenuated complete Freund's adjuvant-induced pain behavior. Further, EA increased pCaMKII-PICK1 complex (abbreviated as C-P complex) levels. Our findings demonstrate that EA inhibits inflammatory pain by inhibiting CaMKII-GluA1 phosphorylation. P-CaMKII is involved in EA analgesia as the pCaMKII-PICK1 complex.

Study Type : Animal Study
Additional Links
Pharmacological Actions : Analgesics : CK(3498) : AC(646)

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