Electroacupuncture Attenuates CFA-Induced Inflammatory Pain by Regulating CaMKII.
Neural Plast
; 2020: 8861994, 2020.
Article
em En
| MEDLINE
| ID: mdl-33488694
ABSTRACT
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.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Dor
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Eletroacupuntura
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Adjuvante de Freund
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Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina
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Manejo da Dor
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article