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  1. 医学部
  1. 医学部
  2. 学術雑誌掲載論文  (医学部)

FK506 causes pain by upregulating NaV1.7 channels in the spinal dorsal root ganglia of NaV1.7-ChR2 mice

http://hdl.handle.net/10458/0002002262
http://hdl.handle.net/10458/0002002262
a50b8e50-adca-471e-85bb-49a0fcc37409
名前 / ファイル ライセンス アクション
maruta-et-al-2026-fk506-causes-pain-by-upregulating-nav1-7-channels-in-the-spinal-dorsal-root-ganglia-of-nav1-7-chr2.pdf Fulltext (958 KB)
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アイテムタイプ 学術雑誌論文 / Journal Article(1)
公開日 2026-02-03
タイトル
タイトル FK506 causes pain by upregulating NaV1.7 channels in the spinal dorsal root ganglia of NaV1.7-ChR2 mice
言語 en
言語
言語 eng
キーワード
言語 en
キーワード FK506
キーワード
言語 en
キーワード NaV1.7
キーワード
言語 en
キーワード calcineurin inhibitor-induced pain syndrome
キーワード
言語 en
キーワード dorsal root ganglion
キーワード
言語 en
キーワード optogenetics
キーワード
言語 en
キーワード tacrolimus
資源タイプ
資源タイプ journal article
アクセス権
アクセス権 open access
著者 丸田, 豊明

× 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

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Shiraishi, Seiji

× Shiraishi, Seiji

en Shiraishi, Seiji(Personal)
Hiroshima University

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興梠, 聡志

× 興梠, 聡志

WEKO 35157
e-Rad_Researcher 00796089

ja 興梠, 聡志
宮崎大学

ja-Kana コウロキ, サトシ

en Kouroki, Satoshi
University of Miyazaki

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Kurogi, Mio

× Kurogi, Mio

en Kurogi, Mio(Personal)
University of Miyazaki

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Hirata, Naoyuki

× Hirata, Naoyuki

en Hirata, Naoyuki(Personal)
Kumamoto University

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抄録
内容記述タイプ Abstract
内容記述 Calcineurin inhibitors, including tacrolimus (FK506), are used as immunosuppressive agents and can cause unexplained calcineurin inhibitor-induced pain syndrome (CIPS). We investigated how FK506 affects the expression of NaV1.7, a voltage-gated Na+ channel implicated in pain perception that is upregulated in dorsal root ganglion (DRG) neurons in several pain disorders. We generated a model of FK506-induced pain by administering FK506 to NaV1.7-ChR2 mice, which exhibit light-responsive pain. To evaluate nociceptive responses, paw withdrawal threshold (PWT) was measured using the von Frey test. The optogenetic place aversion (OPA) and light irradiation paw withdrawal tests were also performed. On the 11th day of initial injection, DRGs were dissected from mice under anesthesia and analyzed for NaV1.7 expression using quantitative reverse transcription PCR (RT-qPCR). PWT was also measured for mice that received the selective NaV1.7 inhibitor or vehicle. PWT was lower in FK506-treated mice than in those administered the vehicle on the 8th and 12th days after initial injection (P < 0.05). Mechanical hypersensitivity was reversible and peaked at around 10 days after FK506 administration. OPA and light irradiation paw withdrawal test results corroborated the hypersensitivity to light-responsivity. NaV1.7 mRNA levels in DRG were higher in FK506-treated mice than in those administered the vehicle on the 11th day (P < 0.05). A selective NaV1.7 inhibitor reversed FK506-induced pain. Increased NaV1.7 expression in DRG neurons may be responsible for FK506-induced peripheral neuropathy. Our findings suggest that endogenous calcineurin regulates NaV1.7 expression. Thus, selective NaV1.7 inhibition could be a potential therapeutic strategy for CIPS.
言語 en
書誌情報 en : Molecular pain

巻 22, p. 17448069251414260, 発行日 2026-01-03
出版者
出版者 SAGE Publications
言語 en
ISSN
収録物識別子タイプ EISSN
収録物識別子 17448069
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 https://doi.org/10.1177/17448069251414260
権利
権利情報 © The Author(s) 2026.
言語 en
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出版タイプ VoR
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