antisense-mediated knockdown of nav1.8, but not nav1.9, generates inhibitory effects on complete freunds adjuvant-induced inflammatory pain in ratnav1.8 antisense-mediated击倒,但不是nav1.9,产生抑制性的影响完全弗氏adjuvant-induced炎性痛大鼠.pdfVIP

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antisense-mediated knockdown of nav1.8, but not nav1.9, generates inhibitory effects on complete freunds adjuvant-induced inflammatory pain in ratnav1.8 antisense-mediated击倒,但不是nav1.9,产生抑制性的影响完全弗氏adjuvant-induced炎性痛大鼠.pdf

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antisense-mediated knockdown of nav1.8, but not nav1.9, generates inhibitory effects on complete freunds adjuvant-induced inflammatory pain in ratnav1.8 antisense-mediated击倒,但不是nav1.9,产生抑制性的影响完全弗氏adjuvant-induced炎性痛大鼠

Antisense-Mediated Knockdown of NaV 1.8, but Not NaV 1.9, Generates Inhibitory Effects on Complete Freund’s Adjuvant-Induced Inflammatory Pain in Rat 1. 1. 2 1,3 Yao-Qing Yu , Feng Zhao , Su-Min Guan *, Jun Chen * 1 Institute for Biomedical Sciences of Pain and Institute for Functional Brain Disorders, Tangdu Hospital, the Fourth Military Medical University, Xi’an, People’s Republic of China, 2 School of Stomatology, the Fourth Military Medical University, Xi’an, People’s Republic of China, 3 Institute for Biomedical Sciences of Pain, Capital Medical University, Beijing, People’s Republic of China Abstract Tetrodotoxin-resistant (TTX-R) sodium channels Na 1.8 and Na 1.9 in sensory neurons were known as key pain modulators. V V Comparing with the widely reported Na 1.8, roles of Na 1.9 on inflammatory pain are poorly studied by antisense-induced V V specific gene knockdown. Here, we used molecular, electrophysiological and behavioral methods to examine the effects of antisense oligodeoxynucleotide (AS ODN) targeting Na 1.8 and Na 1.9 on inflammatory pain. Following complete Freund’s V V adjuvant (CFA) inflammation treatment, Na 1.8 and Na 1.9 in rat dorsal root ganglion (DRG) up-regulated mRNA and V V protein expressions and increased sodium current densities. Immunohistochemical data demonstrated that Na 1.8 mainly