Updated on 2019/05/30
医学博士 ( 1996.3 東京医科歯科大学 )
神経障害性疼痛
難治性疼痛
Life Science / Pathophysiologic neuroscience
Life Science / Pharmacology
Tokyo Medical and Dental University
1992.4 - 1996.3
Country： Japan
Kagoshima University Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area Graduate School of Medical and Dental Sciences Advanced Therapeutics Course Associate Professor
2010.5
日本疼痛学会
2000.4
IASP
1998.4
日本薬理学会
1991.4
日本神経科学会
1990.4
Takasaki I, Nakamura K, Shimodaira A, Watanabe A, Du Nguyen H, Okada T, Toyooka N, Miyata A, Kurihara T . The novel small-molecule antagonist of PAC1 receptor attenuates formalin-induced inflammatory pain behaviors in mice. . J Pharmacol Sci.139 129 - 32 2018.12The novel small-molecule antagonist of PAC1 receptor attenuates formalin-induced inflammatory pain behaviors in mice.Reviewed
Kambe Y, Yokai M, Takasaki I, Kurihara T . Spinal astrocyte-neuron lactate shuttle contributes to the PACAP/PAC1 receptor-induced nociceptive behaviors. . bioRxiv 2018.5Spinal astrocyte-neuron lactate shuttle contributes to the PACAP/PAC1 receptor-induced nociceptive behaviors.
Takasaki I, Watanabe A, Yokai M, Watanabe Y, Hayakawa, D, Nagashima, R, Fukuchi, M, Okada, T, Toyooka, N, Miyata, A, Gouda H, Kurihara T . In silico screening identified novel small-molecule antagonists of PAC1 receptor. . Journal of Pharmacology and Experimental Therapeutics 2018In silico screening identified novel small-molecule antagonists of PAC1 receptor. Reviewed
Aizawa F, Ogaki Y, Kyoya N, Nishinaka T, Nakamoto K, Kurihara T, Hirasawa A, Miyata A, Tokuyama S. . The Deletion of GPR40/FFAR1 Signaling Damages Maternal Care and Emotional Function in Female Mice. . Biol Pharm Bull.40 ( 8 ) 1255 - 1259 2017.8The Deletion of GPR40/FFAR1 Signaling Damages Maternal Care and Emotional Function in Female Mice.Reviewed
Nakamoto K, Aizawa F, Miyagi K, Yamashita T, Mankura M, Koyama Y, Kasuya F, Hirasawa A, Kurihara T, Miyata A, Tokuyama S. . Dysfunctional GPR40/FFAR1 signaling exacerbates pain behavior in mice. . PLoS One 2017.7Dysfunctional GPR40/FFAR1 signaling exacerbates pain behavior in mice.Reviewed
Yuki N, Chan AC, Wong AHY, Inoue T, Yokai M, Kurihara T, Devaux JJ, Wilder-Smith E. . Acute painful autoimmune neuropathy: A variant of Guillain-Barré syndrome. Muscle Nerve. . Muscle Nerve 2017.7Acute painful autoimmune neuropathy: A variant of Guillain-Barré syndrome. Muscle Nerve. Reviewed
Fuka Aizawa, Takashi Nishinaka, Takuya Yamashita, Kazuo Nakamoto, Takashi Kurihara, Akira Hirasawa, Fumiyo Kasuya, Atsuro Miyata, Shogo Tokuyama. . GPR40/FFAR1 deficient mice increase noradrenaline levels in the brain and exhibit abnormal behavior. . Journal of Pharmacological Sciences132 249 - 254 2016.11GPR40/FFAR1 deficient mice increase noradrenaline levels in the brain and exhibit abnormal behavior.Reviewed
Yokai, M., Kurihara, T. & Miyata, A. . Spinal astrocytic activation contributes to both induction and maintenance of pituitary adenylate cyclase-activating polypeptide type 1 receptor-induced long-lasting mechanical allodynia in mice. . Molecular Pain 2016.5Spinal astrocytic activation contributes to both induction and maintenance of pituitary adenylate cyclase-activating polypeptide type 1 receptor-induced long-lasting mechanical allodynia in mice.Reviewed
Ohnou, T., Yokai, M., Kurihara, T., Hasegawa-Moriyama, M., Shimizu, T., Kanmura, Y. & Miyata, A. . Pituitary adenylate cyclase-activating polypeptide type 1 receptor signaling evokes long-lasting nociceptive behaviors through the activation of spinal astrocytes in mice. . Journal of Pharmacological Sciences 2016.2Reviewed
Karki P., Kurihara T., Nakamachi T., Watanabe J., Asada T., Oyoshi T., Shioda S., Yoshimura M., Arita K., Miyata A. . Attenuation of inflammatory and neuropathic pain behaviors in mice through activation of free fatty acid receptor GPR40. . Molecular Pain11 6- 2015.2Attenuation of inflammatory and neuropathic pain behaviors in mice through activation of free fatty acid receptor GPR40.Reviewed
Kurihara, T., Sakurai, E., Toyomoto, M., Kii, I., Kawamoto, D., Asada, T., Tanabe, T., Yoshimura, M., Hagiwara, M. & Miyata, A. . Alleviation of behavioral hypersensitivity in mouse models of inflammatory pain with two structurally different casein kinase 1 (CK1) inhibitors. . Molecular Pain10 17 2014.3Alleviation of behavioral hypersensitivity in mouse models of inflammatory pain with two structurally different casein kinase 1 (CK1) inhibitors.Reviewed
Hanada, T., Kurihara, T., Tokudome, M., Tokimura, H., Arita, K. & Miyata, A. . Development and pharmacological verification of a new mouse model of central post-stroke pain. . Neurosci. Res.78 72 - 80 2014.1Development and pharmacological verification of a new mouse model of central post-stroke pain.Reviewed
Miura, A., Kambe, Y., Inoue, K., Tatsukawa, H., Kurihara, T., Griffin, M., Kojima, S. & Miyata, A. . Pituitary adenylate cyclase-activating polypeptide type 1 receptor (PAC1) gene is suppressed by transglutaminase 2 activation. . Journal of Biological Chemistry288 32720 - 32730 2013.11Pituitary adenylate cyclase-activating polypeptide type 1 receptor (PAC1) gene is suppressed by transglutaminase 2 activation.Reviewed
Miura, A., Odahara, N., Tominaga, A., Inoue, K., Kambe, Y., Kurihara, T. & Miyata, A. . Regulatory mechanism of PAC1 gene expression via Sp1 by nerve growth factor in PC12 cells. . FEBS Lett586 1731 - 1735 2012.1Regulatory mechanism of PAC1 gene expression via Sp1 by nerve growth factor in PC12 cells. Reviewed
Kondo, D., Saegusa, H., Yabe, R., Takasaki, I., Kurihara, T., Zong, S., Tanabe, T. . Peripheral-type benzodiazepine receptor antagonistis effective in relieving neuropathic pain. . J. Pharmacol. Sci.110 55 - 63 2009Peripheral-type benzodiazepine receptor antagonistis effective in relieving neuropathic pain.Reviewed
Sakurai, E., Kurihara, T., Kouchi, K., Saegusa, H., Zong, S., Tanabe, T. . Upregulation of casein kinase 1ε in dorsal root ganglia and spinal cord after mouse spinal nerve injury contributes to neuropathic pain. . Mol. Pain5 74 2009Upregulation of casein kinase 1ε in dorsal root ganglia and spinal cord after mouse spinal nerve injury contributes to neuropathic pain.Reviewed
Kondo, D., Yabe, R., Kurihara, T., Saegusa, H., Zong, S. , Tanabe, T. . Progesteron receptor anatagonist is effective in relieving neuropathic pain. . Eur. J. Pharmacol.541 44 - 48 2006Progesteron receptor anatagonist is effective in relieving neuropathic pain.Reviewed
Takasaki, I., Kurihara, T., Saegusa, H., Zong, S., Tanabe, T. . Effects of glucocorticoid receptor antagonists on allodynia and hyperalgesia in mouse model of neuropathic pain. . Eur. J. Pharmacol.524 80 - 83 2005Effects of glucocorticoid receptor antagonists on allodynia and hyperalgesia in mouse model of neuropathic pain.Reviewed
Yokoyama, K., Kurihara, T., Saegusa, H., Zong, S., Makita, K., Tanabe, T. . Blocking the R-type (Cav2.3) Ca2+ channel enhanced morphine analgesia and reduced morphine tolerance. . Eur. J. Neurosci.20 3516 - 3519 2004Blocking the R-type (Cav2.3) Ca2+ channel enhanced morphine analgesia and reduced morphine tolerance.Reviewed
Kurihara T., Nonaka, T. , Tanabe, T. . Acetic acid-conditioning stimulus induces long-lasting antinociception of somatic inflammatory pain. . Pharmacol. Biochem. Behavior74 841 - 849 2003Acetic acid-conditioning stimulus induces long-lasting antinociception of somatic inflammatory pain. Reviewed
Yokoyama, K., Kurihara, T., Makita, K. , Tanabe, T. . Plastic change of N-type Ca channel expression after preconditioning is responsible for prostaglandin E2-induced long-lasting allodynia. . Anesthesiology99 1364 - 1370 2003Plastic change of N-type Ca channel expression after preconditioning is responsible for prostaglandin E2-induced long-lasting allodynia. Reviewed
Abe M., Kurihara T., Han, W., Shinomiya, K. , Tanabe, T. . Changes in expression of voltage-dependent ion channel subunits in dorsal root ganglia of rats with radicular injury and pain. . Spine27 ( 4 ) 1517 - 1525 2002Changes in expression of voltage-dependent ion channel subunits in dorsal root ganglia of rats with radicular injury and pain.Reviewed
Ogasawara, M., Kurihara, T., Hu, Q. , Tanabe, T. . Characterization of acute somatosensory pain transmission in P/Q-type Ca2+ channel mutant mice, leaner. . FEBS Lett.508 181 - 186 2001Characterization of acute somatosensory pain transmission in P/Q-type Ca2+ channel mutant mice, leaner. Reviewed
Saegusa, H., Kurihara, T., Zong, S., Kazuno, A., Matsuda, Y., Nonaka, T., Han, W., Toriyama, H., Tanabe, T. (H. Saegusa and T. Kurihara contributed equally to this work) . Suppression of inflammatory and neuropathic pain symptoms in mice lacking the N-type Ca2+ channel. . The EMBO Journal20 2349 - 2356 2001Suppression of inflammatory and neuropathic pain symptoms in mice lacking the N-type Ca2+ channel.Reviewed
Sakashita, Y., Kurihara, T., Uchida, D., Tastuno, I., Yamamoto, T. . Involvement of PACAP receptor in primary afferent fibre-evoked responses of ventral roots in the neonatal rat spinal cord. . British Journal of Pharmacology132 1769 - 1776 2001Involvement of PACAP receptor in primary afferent fibre-evoked responses of ventral roots in the neonatal rat spinal cord.Reviewed
Saegusa, H., Kurihara, T., Zong, S., Minowa, O., Kazuno, A., Han, W., Matsuda, Y., Yamanaka, H., Osanai, M., Noda, T., Tanabe, T. . Altered pain responses in mice lacking α1E subunit of the voltage-dependent Ca2+ channel. . Proc. Natl. Acad. Sci. USA97 6132 - 6137 2000Altered pain responses in mice lacking α1E subunit of the voltage-dependent Ca2+ channel. Reviewed
Kurihara, T., Yoshioka, K. . The excitatory and inhibitory modulation of primary afferent fibre-evoked responses of ventral roots in the neonatal rat spinal cord exerted by nitric oxide. . British Journal of Pharmacology118 1743 - 1753 1996The excitatory and inhibitory modulation of primary afferent fibre-evoked responses of ventral roots in the neonatal rat spinal cord exerted by nitric oxide.Reviewed
Otsuka, M., Yoshioka, K., Yanagisawa, M., Suzuki, H., Zhao, F-Y., Guo, J.-Z., Hosoki, R. , Kurihara, T. . Use of NK1 receptor antagonists in the exploration of physiological functions of substance P and neurokinin A. . Canadian Journal of Physiology and Pharmacology73 903 - 907 1995Use of NK1 receptor antagonists in the exploration of physiological functions of substance P and neurokinin A.Reviewed
Kurihara, T., Yoshioka,K., Otsuka, M. . Tachykininergic slow depolarization of motoneurones evoked by descending fibres in the neonatal rat spinal cord. . The Journal of Physiology (London)485 787 - 796 1995Tachykininergic slow depolarization of motoneurones evoked by descending fibres in the neonatal rat spinal cord.Reviewed
Suzuki, H., Yoshioka, K., Yanagisawa, M., Urayama, O., Kurihara, T., Hosoki, R., Saito, K., Otsuka, M. . Involvement of enzymatic degradation in the inactivation of tachykinin neurotransmitters in neonatal rat spinal cord. . British Journal of Pharmacology113 310 - 316 1994Involvement of enzymatic degradation in the inactivation of tachykinin neurotransmitters in neonatal rat spinal cord.Reviewed
Kurihara, T., Suzuki, H., Yanagisawa, M., Yoshioka, K. . Muscarinic excitatory and inhibitory mechanisms involved in afferent fibre-evoked depolarization of motoneurones in the neonatal rat spinal cord. . British Journal of Pharmacology110 61 - 70 1993Muscarinic excitatory and inhibitory mechanisms involved in afferent fibre-evoked depolarization of motoneurones in the neonatal rat spinal cord.Reviewed
Yanagisawa, M., Yoshioka, K., Kurihara, T., Saito, K., Seno, N., Suzuki, H., Hosoki, R. , Otsuka, M. . Enzymatic inactivation of tachykinin neurotransmitters in the isolated spinal cord of the newborn rat. . Neuroscience Research15 289 - 292 1992Enzymatic inactivation of tachykinin neurotransmitters in the isolated spinal cord of the newborn rat.Reviewed
ベッドサイドの薬理学 (笹栗俊之、宮田篤郎 編)
栗原 崇（ Role： Contributor , 第IV編1章1) 鎮痛薬; 1章2) 局所麻酔薬; 1章3) 全身麻酔薬; 1章4) 筋弛緩薬; 第IV編2章1) 頭痛治療薬; 2章2) 抗めまい薬）
丸善出版 2018.3
痛み診療キーポイント. 痛みのScience & Practice 第6巻
栗原 崇（ Role： Sole author , 電位依存性Caチャネル）
分光堂 2014.5
痛み診療キーポイント. 痛みのScience & Practice 第6巻
栗原 崇（ Role： Sole author , グルタミン酸受容体）
分光堂 2014.5
感覚器官と脳内情報処理. シリーズバイオサイエンスの新世紀 第12巻
栗原 崇、 田邊 勉（ Role： Joint author）
共立出版 2002.9
イオンチャネルの分子生物学 (実験医学バイオサイエンスシリーズ28)
村越 隆之、栗原 崇、三枝 弘尚、田邊 勉（ Role： Joint author）
羊土社 1998.12
PACAPシグナリングによって駆動されるアストロサイト―ニューロン乳酸シャトルの中枢神経機能発現への寄与 Reviewed
神戸悠輝，栗原 崇，宮田篤郎
日本薬理学雑誌 151 ( 6 ) 239 - 243 2018.6
Trend & Topics 痛みの分子科学－電位依存性Na+チャネル最前線
栗原 崇
White - これからの女性医療を考える 4 ( 2 ) 42 - 48 2016.9
Involvement of free fatty acid receptor GPR40/FFAR1 in the regulation of spinal nociceptive transmission Reviewed
Folia Pharmacologica Japonica 146 ( 12 ) 309 - 314 2015.12
テトロドトキシン抵抗性Na+チャネルと神経栄養因子BDNF — 新たな疼痛発生機序の可能性 Reviewed
栗原 崇、田邊 勉
日本薬理学雑誌 121 276 2003
疼痛における電位依存性Ca2+チャネルの役割 Reviewed
横山和明、栗原 崇、槙田浩史、田邊 勉
Journal of Neurosciences for Pain Research 5 12 - 20 2003
カルシウムチャネルの構造と機能
栗原 崇、田邊 勉
神経研究の進歩 47 181 - 191 2003
Nタイプカルシウムチャネル Reviewed
栗原 崇、田邊 勉
日本薬理学雑誌 121 211 - 222 2003
神経根性疼痛モデルラット後根神経節における電位依存性イオンチャネルサブユニット発現変化 Reviewed
安部理寛、栗原 崇、韓 文華、四宮謙一、田邊 勉
臨床整形外科 37 ( 4 ) 343 - 349 2002.4
脊髄の伝達物質
栗原 崇、横山和明、田邊 勉.
Clinical Neuroscience 19 761 - 763 2001
痛みとCa2+チャネル Reviewed
栗原 崇、田邊 勉
東京都歯科医師会雑誌 48 473 - 481 2000
電位依存性Ca2+チャネル Reviewed
栗原 崇、田邊 勉
蛋白質核酸酵素 43 1579 - 1588 1998.9
痛覚過敏とNO
栗原 崇、山本達郎
Clinical Neuroscience 16 ( 7 ) 778 - 780 1998.7
電位依存性カルシウムチャネルの分子的多様性: 構造-機能相関と組織特異的発現
栗原 崇、田邊 勉
循環器科 44 1 - 12 1998.7
PAC1受容体拮抗薬を用いた鎮痛薬
栗原 崇、高崎一朗、豊岡尚樹、合田浩明
疼痛に関する化合物及び医薬組成物
萩原正敏、豊本雅靖、細谷孝充、吉田 優、栗原 崇
遊離脂肪酸受容体FFAR1は慢性疼痛に伴ううつ症状発症に関与するのか？
2019.4 - 2022.3
科学研究費補助金 基盤研究(C)
ミクログリアはニューロンに接触して何をしているのか？-疼痛モデルによる解析
2018.3 - 2021.3
科学研究費補助金 基盤研究(C)
アストロサイトPACAP/PAC1Rシグナルが関与する恐怖記憶メカニズムの解明
2017.4 - 2020.3
科学研究費補助金 基盤研究(C)
うつ病におけるミトコンドリア変性タンパク質ストレスレスポンスの関与の解明
2017.4 - 2020.3
科学研究費補助金 基盤研究(C)
新規難治性疼痛治療薬PACAP特異的受容体拮抗薬の実用化研究
2017.4 - 2018.3
国立研究開発法人 日本医療研究開発機構 平成29年度橋渡し研究・新規開発シーズ (シーズA 九州大学公募)
Grant type：Competitive
疼痛・情動行動における脳脊髄FFAR1システムの重要性を検証する
2016.4 - 2019.3
科学研究費補助金 基盤研究(C)
免疫介在性有痛性神経障害発症に関与する病的抗原を同定する
2016.4 - 2018.3
科学研究費補助金 挑戦的萌芽研究
Dectin-1シグナル伝達系を標的にした新規難治性疼痛制御法の開発
2016.4 - 2017.3
その他省庁等 千葉大学真菌医学センター 平成28年度共同利用・共同研究費
Grant type：Competitive
難治性疼痛治療を目指した新規PACAP特異的受容体拮抗薬の開発
2016.4 - 2017.3
国立研究開発法人 日本医療研究開発機構 平成28年度橋渡し研究加速ネットワークプログラムシーズA
Grant type：Competitive
脳卒中後疼痛・情動異常発症メカニズムの検討 ― 「ミクログリア活性化仮説
2015.4 - 2018.3
科学研究費補助金 基盤研究(C)
PACAP-PAC1誘発アストロサイトシグナル伝達を標的とする慢性疼痛治療戦略
2014.4 - 2017.3
科学研究費補助金 基盤研究(C)
新規脂肪酸受容体GPR40を介する疼痛抑制メカニズムの研究
2013.4 - 2016.3
科学研究費補助金 基盤研究(C)
カゼインキナーゼ1シグナル伝達系をターゲットにした難治性疼痛治療戦略
2013.4 - 2016.3
科学研究費補助金 基盤研究(C)
視床痛モデルマウスの確立と視床痛発症メカニズムの基礎的検討
2012.4 - 2015.3
科学研究費補助金 基盤研究(C)
新規疼痛関連リン酸化酵素情報伝達マップ: リン酸化プロテオミクスによる痛み表情解析
2010.4 - 2013.3
科学研究費補助金 基盤研究(C)
オピオイド系鎮痛薬の生体作用における神経型カルシウムチャネルの役割
2007.4 - 2010.3
科学研究費補助金 基盤研究(C)
電位依存性Ca2+チャネル遺伝子変異マウスを用いた痛覚情報伝達メカニズムの研究
2002.4 - 2005.3
科学研究費補助金 若手研究(A)
神経障害性疼痛により後根神経節において発現変化を受ける遺伝子群の検索
1999.4 - 2002.3
科学研究費補助金 基盤研究(C)
アンチセンス法を用いた脊髄痛覚伝達・増強機構に関与するG蛋白質の解析
1997.4 - 1999.3
科学研究費補助金 奨励研究
新生ラット摘出脊髄標本を用いた痛覚伝達機構の研究
1993.4 - 1996.3
科学研究費補助金 特別研究員奨励費
