Electroacupuncture Attenuates CFA-Induced Inflammatory Pain by Regulating CaMKII

• Published in: Journal of neural transplantation & plasticity Vol. 2020; no. 2020; pp. 1 - 12
• Main Authors: Wang, Junlu, Dai, Qinxue, Li, Shan, Zhao, Xiaoyong, Chen, Na, Tu, Yingying, Mo, Yunchang, Chen, Shuangdong, Gu, Yixiao, Yu, Qimin
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 2020; Hindawi; John Wiley & Sons, Inc; Hindawi Limited; Wiley
• Subjects: Acupuncture; Analgesics; Analysis; Behavior; Calcium-binding proteins; Care and treatment; Electroacupuncture; Fluorides; Health aspects; Kinases; Laboratory animals; Life sciences; Membranes; Pain; Protein kinases; Proteins; United Kingdom; China; Beijing China; United Kingdom > UK; United States > US
• ISSN: 2090-5904; 0792-8483; 1687-5443
• DOI: 10.1155/2020/8861994

Ca2+/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.