| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2025-07-21 |
| タイトル |
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タイトル |
Reversible neuropathic pain model created by long-term optogenetic nociceptor stimulation using light-responsive pain mice |
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言語 |
en |
| 言語 |
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言語 |
eng |
| 資源タイプ |
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資源タイプ |
journal article |
| アクセス権 |
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アクセス権 |
open access |
| 著者 |
Kouroki, Satoshi
丸田, 豊明
WEKO
34465
e-Rad_Researcher
20363591
| ja |
丸田, 豊明
宮崎大学
|
| ja-Kana |
マルタ, トヨアキ
|
| en |
Maruta, Toyoaki
University of Miyazaki
|
Search repository
日髙, 康太郎
WEKO
34788
e-Rad_Researcher
20750392
| ja |
日髙, 康太郎
宮崎大学
|
| ja-Kana |
ヒダカ, コウタロウ
|
| en |
Hidaka, Kotaro
University of Miyazaki
|
Search repository
越田, 智広
WEKO
34811
e-Rad_Researcher
20441842
| ja |
越田, 智広
宮崎大学
|
| ja-Kana |
コシダ, トモヒロ
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| en |
Koshida, Tomohiro
University of Miyazaki
|
Search repository
黒木, 未央
鹿毛, 陽子
三浦, 綾子
WEKO
21756
e-Rad_Researcher
70710903
| ja |
三浦, 綾子
宮崎大学
|
| ja-Kana |
ミウラ, アヤコ
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| en |
Miura, Ayako
University of Miyazaki
|
Search repository
中川, 光
WEKO
35310
| ja |
中川, 光
宮崎大学
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| ja-Kana |
ナカガワ, ヒカル
|
| en |
Nakagawa, Hikaru
University of Miyazaki
|
Search repository
柳田, 俊彦
WEKO
7906
e-Rad_Researcher
60295227
| ja |
柳田, 俊彦
宮崎大学
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| ja-Kana |
ヤナギタ, トシヒコ
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| en |
Yanagita, Toshihiko
University of Miyazaki
|
Search repository
武谷, 立
恒吉, 勇男
WEKO
8080
e-Rad_Researcher
90301390
| ja |
恒吉, 勇男
宮崎大学
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| ja-Kana |
ツネヨシ, イサオ
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| en |
Tsuneyoshi, Isao
University of Miyazaki
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Search repository
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| 抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Neuropathic pain has a significant social impact, with high morbidity and reduced productivity, the underlying mechanisms of neuropathic pain remain poorly understood, and effective therapeutic strategies remain elusive. The development of animal models of neuropathic pain that stimulate only the nociceptors and not the other sensory receptors or motor nerves is desirable for elucidating the complex pathogenesis of neuropathic pain. We have previously reported the generation of NaV1.7−channelrhodopsin-2 (ChR2), NaV1.8−ChR2, and NaV1.9−ChR2 mice. Optogenetics was employed in these light-responsive pain mice for generating nociceptive pain by specifically exciting the spinal dorsal root ganglion neurons, in which the respective Na+ channels are expressed through exposure to blue light. This study aimed to compare the neuropathic pain produced by the prolonged exposure of light-responsive pain mice to blue light. A reversible neuropathic pain state was established persisting for a minimum of 24 hours when each light-responsive pain mouse was irradiated with light of an intensity that consistently elicited pain. Furthermore, the mice also showed pain sensitivity to light irradiation and mechanical stimulation. The expression of c-Fos, a marker for neuronal activity following noxious stimulation, was increased in the dorsal horn of the spinal cord on the light irradiated side. DS-1971a, a selective NaV1.7 inhibitor, was effective in attenuating neuropathic pain in all light-responsive pain mice. In conclusion, optogenetics helps elucidate the specific functions of sodium channel subtypes in pain signaling, thereby advancing our understanding and paving the way for the development of further effective treatments for pain disorders in the future. |
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言語 |
en |
| 書誌情報 |
en : Plos One
巻 20,
号 5,
p. e0323628,
発行日 2025-05-30
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| 出版者 |
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出版者 |
Public Library of Science (PLoS) |
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言語 |
en |
| ISSN |
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収録物識別子タイプ |
EISSN |
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収録物識別子 |
19326203 |
| DOI |
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関連タイプ |
isVersionOf |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.1371/journal.pone.0323628 |
| 著者版フラグ |
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出版タイプ |
VoR |
Fulltext (1 MB)
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