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KAKEN_22390182seika.pdf
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Title |
Title |
片頭痛前兆大脳皮質拡延性抑制が神経障害性疼痛を惹起する脳可塑性と疼痛制御系の解明
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Kana |
ヘンズツウ ゼンチョウ ダイノウ ヒシツ カクエンセイ ヨクセイ ガ シンケイ ショウガイセイ トウツウ オ ジャッキスル ノウ カソセイ ト トウツウ セイギョケイ ノ カイメイ
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Henzutsu zencho daino hishitsu kakuensei yokusei ga shinkei shogaisei totsu o jakkisuru no kasosei to totsu seigyokei no kaimei
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Research on migraine pathophysiology related to cortical spreading depression
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鈴木, 則宏
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Kana |
スズキ, ノリヒロ
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Romanization |
Suzuki, Norihiro
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Affiliation |
慶應義塾大学・医学部・教授
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Research team head
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科研費研究者番号 : 10158975
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清水, 利彦
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Kana |
シミズ, トシヒコ
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Romanization |
Shimizu, Toshihiko
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Affiliation |
慶應義塾大学・医学部・講師
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Research team member
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科研費研究者番号 : 40265799
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柴田, 護
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シバタ, マモル
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Shibata, Mamoru
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Affiliation |
慶應義塾大学・医学部・講師
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Research team member
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科研費研究者番号 : 60286466
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鳥海, 春樹
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トリウミ, ハルキ
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Toriumi, Haruki
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慶應義塾大学・医学部・講師(非常勤)
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Research team member
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科研費研究者番号 : 30528203
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小泉, 健三
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コイズミ, ケンゾウ
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Romanization |
Koizumi, Kenzo
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慶應義塾大学・医学部・助教
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Research team member
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科研費研究者番号 : 30439070
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舟久保, 恵美
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フナクボ, メグミ
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Romanization |
Funakubo, Megumi
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慶應義塾大学・医学部・講師(非常勤)
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Research team member
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科研費研究者番号 : 90548538
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2015
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科学研究費補助金研究成果報告書
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2014
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Abstract |
皮質拡延性抑制(CSD)が片頭痛の病態に及ぼす影響を検討した。CSD誘発は三叉神経節においてTRPV1受容体を介しERKのリン酸化を引き起すこと, 大脳皮質の神経細胞において炎症性疼痛発生と関連の深いDAMPs(damage-associated molecular patterns)の1つであるHMGB1の転写誘導および細胞外放出をCSDの発現する回数に依存的に亢進させることを明らかにした。さらに三叉神経節ニューロンではTRPV1の刺激によりカスパーゼ依存性のアポトーシスが誘導された。これらの結果はCSDが神経障害性疼痛を惹起する脳可塑性と疼痛制御系を解明していく上で有用な知見と考えらえた。
We explored the relationship between cortical spreading depression (CSD) and the trigeminovascular system. This study revealed that nociceptive stimulation of the dura mater and CSD increased the level of ERK phosphorylation in the trigeminal system, and indicated that CSD can activate the trigeminal system. CSD has also been shown to induce the release of the nuclear protein termed high-mobility group box 1 (HMGB1) from neurons, causing activation of the trigeminovascular system. We explored the effects of CSD inductions on HMGB1 transcriptional activity, and revealed that CSD up-regulates HMGB1 transcriptional activity in neurons, but not in astrocytes. CSD also induced the release of HMGB1 from neurons, but not astrocytes. The magnitude of these alterations depends on the number of CSD inductions. Moreover, TRPV1 stimulation caused caspase-dependent apoptotic cell death of trigeminal ganglion neurons. These data provide important clues regarding the pathophysiology of migraine.
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研究種目 : 基盤研究(B)
研究期間 : 2010~2014
課題番号 : 22390182
研究分野 : 医歯薬学
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