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Faculty of Medicine College Hospital Anesthesiology |
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Assistant Professor |
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Related SDGs |
Papers 【 display / non-display 】
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文献抄訳:Clinical research on the effectiveness and safety of Uchasingihwan for low back pain with radiculopathy caused by ferniated intervertebral disc of the lumbar spine: a multicenter, randomized, controlled equivalence trial. Reviewed
児玉芳史,日髙康太郎,恒吉勇男
ペインクリニック 46 ( 9 ) 1009 - 1010 2025.9
Language:Japanese Publishing type:Research paper (scientific journal)
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Reversible neuropathic pain model created by long-term optogenetic nociceptor stimulation using light-responsive pain mice. Reviewed
Satoshi Kouroki, Toyoaki Maruta, Kotaro Hidaka, Tomohiro Koshida, Mio Kurogi, Yohko Kage, Syako Miura, Hikarru Nakagawa, Toshihiko Yanagita, Ryu Takeya, Isao Tsuneyoshi
PLoS One 20 ( 5 ) e0323628 2025.5
Language:English Publishing type:Research paper (scientific journal)
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Maruta T., Kouroki S., Kurogi M., Hidaka K., Koshida T., Miura A., Nakagawa H., Yanagita T., Takeya R., Tsuneyoshi I.
Journal of Neuroscience Research 102 ( 10 ) e25386 2024.10
Language:English Publishing type:Research paper (scientific journal) Publisher:Journal of Neuroscience Research
Voltage-gated sodium channels, including NaV1.7, NaV1.8, and NaV1.9, play important roles in pain transmission and chronic pain development. However, the specific mechanisms of their action remain unclear, highlighting the need for in vivo stimulation studies of these channels. Optogenetics, a novel technique for targeting the activation or inhibition of specific neural circuits using light, offers a promising solution. In our previous study, we used optogenetics to selectively excite NaV1.7-expressing neurons in the dorsal root ganglion of mice to induce nocifensive behavior. Here, we further characterize the impact of nocifensive behavior by activation of NaV1.7, NaV1.8, or NaV1.9-expressing neurons. Using CRISPR/Cas9-mediated homologous recombination, NaV1.7–iCre, NaV1.8–iCre, or NaV1.9–iCre mice expressing iCre recombinase under the control of the endogenous NaV1.7, NaV1.8, or NaV1.9 gene promoter were produced. These mice were then bred with channelrhodopsin-2 (ChR2) Cre–reporter Ai32 mice to obtain NaV1.7–ChR2, NaV1.8–ChR2, or NaV1.9–ChR2 mice. Blue light exposure triggered paw withdrawal in all mice, with the strongest response in NaV1.8–ChR2 mice. These light sensitivity differences observed across NaV1.x–ChR2 mice may be dependent on ChR2 expression or reflect the inherent disparities in their pain transmission roles. In conclusion, we have generated noninvasive pain models, with optically activated peripheral nociceptors. We believe that studies using optogenetics will further elucidate the role of sodium channel subtypes in pain transmission.
DOI: 10.1002/jnr.25386
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【各種難治性疼痛に対する最新治療】下肢の虚血性疼痛に対する脊髄刺激療法. Reviewed
立山慎吾,日髙康太郎
ペインクリニック 45 ( 7 ) 717 - 718 2024.7
Language:Japanese Publishing type:Research paper (scientific journal)
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Koshida T., Maruta T., Tanaka N., Hidaka K., Kurogi M., Nemoto T., Yanagita T., Takeya R., Tsuneyoshi I.
Acta Medica Okayama 77 ( 4 ) 359 - 364 2023
Language:English Publishing type:Research paper (scientific journal) Publisher:Acta Medica Okayama
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.
DOI: 10.18926/AMO/65741
Presentations 【 display / non-display 】
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低左心機能を合併した重症大動脈弁狭窄症に対し,準緊急でVA-ECMO補助下にTAVIを施行した1例.
児玉芳史,永田悠紀子,日髙康太郎,恒吉勇男
第38回日本老年麻酔学会学術集会 2026.2.28
Event date: 2026.2.28
Language:Japanese Presentation type:Oral presentation (general)
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帯状疱疹に伴う神経痛に対し桂枝加朮附湯の効果を認めた症例と認めなかった症例.
日髙康太郎
第9回九州・沖縄・山口「痛みと漢方を学ぶ会」学術集会 2026.1.24
Event date: 2026.1.24
Language:Japanese Presentation type:Oral presentation (general)
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「自分自身の予後」に対する誤解の解消によりオピオイド必要量が激減した1症例.
末田光恵,小池香苗,日髙麻希,西村亜希,湯淺由佳,谷之木佑歌,畑中真理,前田充範,赤松有希子,押川 隆,藤元貴子,日髙弘登,日髙康太郎,丸田豊明,船橋英樹,山賀昌治,藤永映人,村嶋隆哉,細川 歩
日本緩和医療学会第7回九州支部学術大会 2025.10.15
Event date: 2025.10.15
Language:Japanese Presentation type:Poster presentation
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Currarino症候群による肛門部痛・臀部痛に脊髄刺激療法が著効した1例.
立山真吾,山賀昌治,日髙康太郎
日本ペインクリニック学会第59回学術集会 2025.7
Event date: 2025.7.10 - 2025.7.12
Language:Japanese Presentation type:Oral presentation (general)
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脊髄刺激療法の問題点を打破した4例の解析.
立山真吾,日髙康太郎
日本ペインクリニック学会第59回学術集会 2025.7
Event date: 2025.7.10 - 2025.7.12
Language:Japanese Presentation type:Oral presentation (general)
Grant-in-Aid for Scientific Research 【 display / non-display 】
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NaV1.7を標的とする疼痛治療薬の光遺伝学的探索:トラマドールとミロガバリン
Grant number:23K15603 2023.04 - 2026.03
独立行政法人日本学術振興会 科学研究費基金 若手研究
Authorship:Principal investigator