CC chemokine ligand 2 (CCL2)enhances TTX-sensitive sodium channel activity of primary afferent neurons in the complete Freud adjuvant-induced inflammatory pain model

查看全文 作　　者：Ping [1]Luo;Jiayun [2]Shao;Yingfu [2]Jiao;Weifeng [2]Yu;Weifang [1]Rong

机构地区：[1]Department of Anatomy and Physiology,Shanghai Jiaotong University School of Medicine,Shanghai 200025 China;[2]Department of Anesthesiology,Renji Hospital,School of Medicine,Shanghai Jiaotong University Shanghai 200127,China

出　　处：《Acta Biochimica et Biophysica Sinica》索引2018年第50卷第12期,共8页

基　　金：the grant from the National Natural Science Foundation of China(No.81270464). 摘　　要：CC chemokine ligand 2 (CCL2)has been implicated in pathological pain,but the mechanism underlying the pronociceptive effect of CCL2 is not fully understood.Voltage-gated sodium (Nav)channels are important determinants of the excitability of sensory neurons.Hence we tested the hypothesis that CCL2 contributes to inflammatory pain via modulating Nay channel activity of primary afferent neurons. Chronic inflammatory pain was induced in rats by intraplantar injection of the complete Freud adjuvant (CFA)to one of the hind paws.Control rats received intraplantar injection of equal volume of saline.A significant increase of CCL2 mRNA and CCL2 receptor (CCR2)protein expression was detected in the ipsilateral dorsal root ganglion (DRG)in CFA-treated rats.lntrapiantar injection of CCL2 protein in the control rats had minimal effect on the paw withdrawal threshold (PWT)in response to mechanical stimulation.However,in CFA-treated rats,intraplantar CCL2 led to an increase in pain responses.Patchclamp recording of acutely dissociated DRG neurons revealed that CCL2 had minimum effect on the excitability of sensory neurons from control rats.However,CCL2 directly depolarized a large proportion of small to medium-sized sensory neurons from CFA-treated rats.In addition,CCL2 was found to enhance whole-cell TTX-sensitive sodium currents without significantly affecting the TTX-resistant sodium currents and the potassium currents.These results are in agreement with previous reports concerning the involvement of CCL2-CCR2 signaling in inflammatory hyperalgesia and further indicate that enhanced TTX-sensitive channel activity may partly underlie the pronociceptive effects of CCL2. 关键词：INFLAMMATORY pain CCL2 CCR2 VOLTAGE-GATED sodium channel potassium channe

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CC chemokine ligand 2 (CCL2)enhances TTX-sensitive sodium channel activity of primary afferent neurons in the complete Freud adjuvant-induced inflammatory pain model

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