Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia

Abstract

Several voltage-gated sodium channels (Navs) from nociceptive nerve fibers have been identified as important effectors in pain signaling. The objective of this study is to investigate the electroacupuncture (EA) analgesia mechanism by changing the expression of Navs in mice dorsal root ganglia (DRG). We injected carrageenan and complete Freund's adjuvant (CFA) into the mice plantar surface of the hind paw to induce inflammation and examined the antinociception effect of EA at the Zusanli (ST36) acupoint at 2 Hz low frequency. Mechanical hyperalgesia was evaluated by using electronic von Frey filaments, and thermal hyperalgesia was assessed using Hargreaves' test. Furthermore, we observed the expression and quality of Navs in DRG neurons. Our results showed that EA reduced mechanical and thermal pain in inflammatory animal model. The expression of Nav1.7 and Nav1.8 was increased after 4 days of carrageenan- and CFA-elicited inflammatory pain and further attenuated by 2 Hz EA stimulation. The attenuation cannot be observed in Nav1.9 sodium channels. We demonstrated that EA at Zusanli (ST36) acupoint at 2 Hz low-frequency stimulation attenuated inflammatory pain accompanied by decreasing the expression of Nav1.7 and 1.8, rather than Nav1.9, sodium channels in peripheral DRG neurons.

Chitosan Oligosaccharide Reduces Propofol Requirements and Propofol-Related Side Effects

“…CFA increasing the expression of Nav1.7 was also reported in an earlier study [49]. CFA increased the colocalization of protein kinase B/Akt with Nav1.7 in L4/5 DRG neurons while Akt pathway induced the upregulation of Nav1.7 [50].…”

“…According to a previous report, CFA infection increases the expression of Nav1.7 [49]. Nav1.7 can be upregulated in L4/5 DRG neurons in a certain evoking situation [50].…”

Colonic Hypersensitivity and Sensitization of Voltage-gated Sodium Channels in Primary Sensory Neurons in Rats with Diabetes

“…Two isoforms of the α-subunit of VGSCs, Na V 1.7, and Na V 1.8, are expressed at high levels in nociceptive sensory neurons. 8 Multiple lines of evidence show that they have been implicated in the development of inflammatory pain 9,10 and neuropathic pain. [11][12][13] Furthermore, dysregulation of VGSCs in injured sensory neurons is also involved in the development of painful peripheral neuropathy in a rat model of diabetes.…”

Identification of WB4101, anα1-Adrenoceptor Antagonist, as a Sodium Channel Blocker

“…The two subtypes of sodium channels are mainly distributed in dorsal root ganglion neurons and have been recognized as important drug targets for pain (Black et al, 2004;Huang et al, 2013;Liang et al, 2013). Therefore to illustrate the mechanism of WB4101 on sodium channels, we tested the effect of WB4101 on recombinant sodium channel subtypes Nav1.7 and Nav1.8.…”