Activation of the N-methyl-D-aspartate receptor and calcium/calmodulin-dependent protein kinase IIα signal in the rostral anterior cingulate cortex is involved in pain-related aversion in rats with peripheral nerve injury

Gao, Xueqi; Lin, Jinhai; Sun, Lin; Hu, Jun; Gao, Wenjie; Yu, Jianfeng

doi:10.1016/j.bbr.2023.114560

Cited by 1 publication

(1 citation statement)

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“…CaMKII is formed by 12 catalytically active subunits [ 10 ], each encoded by 4 genes [ 11 ]. As a reaction to Ca 2+ elevations induced by extracellular stimulation, CaMKII at the 286 threonine position (Thr286) is self-phosphorylated by the adjacent kinase domain and has Ca 2+ -independent activity [ 12 , 13 ]. Self-phosphorylation of CaMKIIα continues to activate enzymes and downstream pathways efficiently even after injury-induced calcium influx [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Electroacupuncture alleviates streptozotocin-induced diabetic neuropathic pain via suppressing phosphorylated CaMKIIα in rats

Li,

Zheng,

Kang

et al. 2024

NeuroReport

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Diabetic neuropathic pain (DNP) is a frequent complication of diabetes. Calcium/calmodulin-dependent protein kinase II α (CaMKIIα), a multi-functional serine/threonine kinase subunit, is mainly located in the surface layer of the spinal cord dorsal horn (SCDH) and the primary sensory neurons in dorsal root ganglion (DRG). Numerous studies have indicated electroacupuncture (EA) takes effect in various kinds of pain. In this research, we explored whether CaMKIIα on rats’ SCDH and DRG participated in DNP and further explored the mechanisms underlying the analgesic effects of EA. The DNP model in rats was successfully established by intraperitoneal injection of streptozotocin. Certain DNP rats were treated with intrathecal injections of KN93, a CaMKII antagonist, and some of the DNP rats received EA intervention. The general conditions, behaviors, the expressions of CaMKIIα and phosphorylated CaMKIIα (p-CaMKIIα) were evaluated. DNP rats’ paw withdrawal threshold was reduced and the expressions of p-CaMKIIα in SCDH and DRG were upregulated compared with the Normal group, while the level of CaMKIIα showed no significance. KN93 attenuated DNP rats’ hyperalgesia and reduced the expressions of p-CaMKIIα. We also found EA attenuated the hyperalgesia of DNP rats and reduced the expressions of p-CaMKIIα. The above findings suggest that p-CaMKIIα in SCDH and DRG is involved in DNP. The analgesic effect of EA in DNP might be related to the downregulation of p-CaMKIIα expression level. Our study further supports that EA can be an effective clinical treatment for DNP.

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