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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
Abstract
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.
Keywords
pulsed radiofrequency
resiniferatoxin
transient receptor potential vanilloid subtype-1 (TRPV1)
calcitonin gene-related peptide (CGRP)
brain-derived neurotrophic factor (BDNF)
Amo Type
Original Article
Publication Title
Acta Medica Okayama
Published Date
2023-08
Volume
volume77
Issue
issue4
Publisher
Okayama University Medical School
Start Page
359
End Page
364
ISSN
0386-300X
NCID
AA00508441
Content Type
Journal Article
language
English
Copyright Holders
Copyright Ⓒ 2023 by Okayama University Medical School
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publisher
Refereed
True
PubMed ID
Web of Science KeyUT