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ID 65741
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著者
Koshida, Tomohiro Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
Maruta, Toyoaki Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
Tanaka, Nobuhiko Tanaka homecare clinic
Hidaka, Kotaro Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
Kurogi, Mio Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
Nemoto, Takayuki Department of Pharmacology, Faculty of Medicine, Fukuoka University
Yanagita, Toshihiko Department of Clinical Pharmacology, School of Nursing, Faculty of Medicine, University of Miyazaki
Takeya, Ryu Department of Pharmacology, Faculty of Medicine, University of Miyazaki
Tsuneyoshi, Isao Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
抄録
Pulsed radiofrequency (PRF) is a safe method of treating neuropathic pain by generating intermittent electric fields at the needle tip. Resiniferatoxin (RTX) is an ultrapotent agonist of transient receptor potential vanilloid subtype-1 (TRPV1) receptors. We investigated the mechanism of PRF using a rat model of RTX-induced neuropathic pain. After administering RTX intraperitoneally, PRF was applied to the right sciatic nerve. We observed the changes in TRPV1, calcitonin gene-related peptide (CGRP), and brain-derived neurotrophic factor (BDNF) in the dorsal root ganglia by western blotting. Expressions of TRPV1 and CGRP were significantly lower in the contralateral (RTX-treated, PRF-untreated) tissue than in control rats (p<0.0001 and p<0.0001, respectively) and the ipsilateral tissues (p<0.0001 and p<0.0001, respectively). BDNF levels were significantly higher in the contralateral tissues than in the control rats (p<0.0001) and the ipsilateral tissues (p<0.0001). These results suggest that, while TRPV1 and CGRP are decreased by RTX-induced neuronal damage, increased BDNF levels result in pain development. PRF may promote recovery from neuronal damage with concomitant restoration of TRPV1 and CGRP, and exert its analgesic effect by reversing BDNF increase. Further research is required to understand the role of TRPV1 and CGRP restoration in improving mechanical allodynia.
キーワード
pulsed radiofrequency
resiniferatoxin
transient receptor potential vanilloid subtype-1 (TRPV1)
calcitonin gene-related peptide (CGRP)
brain-derived neurotrophic factor (BDNF)
Amo Type
Original Article
出版物タイトル
Acta Medica Okayama
発行日
2023-08
77巻
4号
出版者
Okayama University Medical School
開始ページ
359
終了ページ
364
ISSN
0386-300X
NCID
AA00508441
資料タイプ
学術雑誌論文
言語
英語
著作権者
Copyright Ⓒ 2023 by Okayama University Medical School
論文のバージョン
publisher
査読
有り
PubMed ID
Web of Science KeyUT