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  1. 研究者リスト
  2. 小野 秀樹

小野 秀樹

オノ ヒデキ  (ONO HIDEKI)

基本情報

所属
武蔵野大学 薬学部 薬学科 教授
学位
薬学博士(東京大学)
J-GLOBAL ID
200901084214854756
researchmap会員ID
1000212505

研究キーワード

 5

研究分野

 1

経歴

 11
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学歴

 2

委員歴

 16
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論文

 171
  • 小野秀樹
    YAKUGAKU ZASSHI 139(5) 767-781 2019年5月1日  査読有り筆頭著者
  • 小野秀樹, 岡村 真彩, 福島 章紘
    YAKUGAKU ZASSHI 138(9) 1201-1215 2018年9月1日  査読有り筆頭著者
  • Akihiro Fukushima, Arisa Fukui, Yuki Takemura, Yasuhiro Maeda, Hideki Ono
    Journal of pharmacological sciences 136(1) 39-41 2018年1月  査読有り
    Oseltamivir has a hypothermic effect in mice when injected intraperitoneally (i.p.) and intracerebroventricularly (i.c.v.). Here we show that the hypothermia evoked by i.c.v.-oseltamivir is inhibited by non-selective dopamine receptor antagonists (sulpiride and haloperidol) and the D2-selective antagonist L-741,626, but not by D1/D5-selective and D3-selective antagonists (SCH-23390 and SB-277011-A, respectively). The hypothermic effect of i.p.-administered oseltamivir was not inhibited by sulpiride, haloperidol, L-741,626 and SCH-23390. In addition, neither sulpiride, haloperidol nor SCH-23390 blocked hypothermia evoked by i.c.v.-administered oseltamivir carboxylate (a hydrolyzed metabolite of oseltamivir). These results suggest that oseltamivir in the brain induces hypothermia through activation of dopamine D2 receptors.
  • Akihiro Fukushima, Kizuku Mamada, Aki Iimura, Hideki Ono
    Scientific Reports 7(1) 2017年12月1日  査読有り
    The transient receptor potential vanilloid type 1 (TRPV1) is a thermosensitive cation channel that triggers heat pain in the periphery. Long-term desensitization of TRPV1, which can be induced by excess amounts of agonists, has been a method for investigating the physiological relevance of TRPV1-containing neuronal circuits, and desensitization induced by various routes of administration, including systemic, intrathecal and intraganglionic, has been demonstrated in rodents. In the present study, we examined the effect of intracerebroventricular (i.c.v.) treatment with an ultrapotent TRPV1 agonist, resiniferatoxin (RTX), on nociception and the analgesic effect of acetaminophen, which is known to mediate the activation of central TRPV1. I.c.v. administration of RTX a week before the test did not affect the licking/biting response to intraplantar injection of RTX (RTX test), suggesting that such i.c.v. treatment spares the function of TRPV1 at the hindpaw. Mice that had been i.c.v.-administered RTX also exhibited normal nociceptive responses in the formalin test and the tail pressure test, but acetaminophen failed to induce analgesia in those mice in any of the tests. These results suggest that i.c.v. administration of RTX leads to brain-selective TRPV1 desensitization in mice.
  • Akihiro Fukushima, Wakana Sekiguchi, Kizuku Mamada, Yumi Tohma, Hideki Ono
    BIOLOGICAL & PHARMACEUTICAL BULLETIN 40(2) 227-233 2017年2月  査読有り
    Acetaminophen (AcAP), a widely-used antipyretic and analgesic drug, has been considered to exert its effects via central mechanisms, and many studies have demonstrated that the analgesic action of AcAP involves activation of the serotonergic system. Although the serotonergic system also plays an important role in thermoregulation, the contribution of serotonergic activity to the hypothermic effect of AcAP has remained unclear. In the present study, we examined whether the serotonergic system is involved in AcAP-induced hypothermia. In normal mice, AcAP (300 mg/kg, intraperitoneally (i.p.)) induced marked hypothermia (ca. -4 degrees C). The same dose of AcAP reduced pain response behavior in the formalin test. Pretreatment with the serotonin synthesis inhibitor DL-p-chlorophenylalanine (PCPA, 300 mg/kg/d, i.p., 5 consecutive days) substantially decreased serotonin in the brain by 70% and significantly inhibited the analgesic, but not the hypothermic action of AcAP. The same PCPA treatment significantly inhibited the hypothermia induced by the selective serotonin reuptake inhibitor fluoxetine hydrochloride (20mg/kg, i.p.) and the serotonin 5-HT2 receptor antagonist cyproheptadine hydrochloride (3 mg/kg, i.p.). The lower doses of fluoxetine hydrochloride (3 mg/kg, i.p.) and cyproheptadine hydrochloride (0.3 mg/kg, i.p.) did not affect the AcAP-induced hypothermia. These results suggest that, in comparison with its analgesic effect, the hypothermic effect of AcAP is not mediated by the serotonergic system.
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MISC

 93
  • Masahiro Ohsawa, Shohei Yamamoto, Hideki Ono
    YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN 134(3) 387-395 2014年3月  
    Central sensitization in the spinal cord is well known to be involved in chronic pain. Recent investigations indicated that the protein expressions involving the synaptic plasticity are changed in several brain areas under a chronic pain condition. These changes in supraspinal neural function might cause the emotional and memory dysfunction. It is also possible that these changes are involved in the chronic pain. Indeed, since the improvement of spinal and peripheral sensitization showed limited relief in the neuropathic pain, the sensitization of supraspinal nociceptive transmission might be involved in the expression of chronic pain. We recently found that intra-thalamic treatment with excitatory neurotransmitter glutamate caused hyperalgesia, which is mediated by the stimulation of glutamate N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Moreover, intracerebroventricular treatment with gabapentin, a calcium channel alpha2delta-1 subunit blocker, attenuated the hyperalgesia in the nerve-injury model of mice. These results suggest that the sensitization of supraspinal nociceptive transmission is involved in neuropathic pain. It is also indicated that neuropathic pain is resulted from the activations of spinal glial cells. Likewise, the supraspinal glial activation was observed in the neuropathic pain. Therefore, the sensitization of supraspinal nociceptive transmission might be important for a chronic pain. In this review, we would like to discuss the possible involvement of the supraspinal sensitization in neuropathic pain and in its application for the curative treatment in chronic pain.
  • Masahiro Ohsawa, Riyo Nakamura, Noboru Inoue, Tomoyasu Murakami, Hiroki Katsu, Shohei Yamamoto, Hideki Ono
    DIABETES 62 A211-A212 2013年7月  
  • Yu Masegi, Hideki Ono, Mitsuo Tanabe
    JOURNAL OF PHARMACOLOGICAL SCIENCES 118 194P-194P 2012年  
  • Seiya Kuraoka, Hideki Ono, Mitsuo Tanabe
    JOURNAL OF PHARMACOLOGICAL SCIENCES 118 193P-193P 2012年  
  • Saki Otake, Shohei Yamamoto, Masahiro Ohsawa, Masahide Noji, Hideki Ono
    JOURNAL OF PHARMACOLOGICAL SCIENCES 118 146P-146P 2012年  
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書籍等出版物

 32
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講演・口頭発表等

 21
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所属学協会

 15
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Works(作品等)

 4

共同研究・競争的資金等の研究課題

 20
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社会貢献活動

 5

教育内容・方法の工夫

 2
  • 件名
    認定実務実習指導薬剤師養成ワークショップ in 東海　タスクフォース
    年月日（From)
    2005/12
    年月日（To）
    2008
    概要
    第1回、4回、5回、12回ワークショップにおいて、タスクフォースを務めた。
  • 件名
    文科省戦略的大学連携支援事業「6年制薬学教育を主軸とする薬系・医系・看護系大学による広域総合教育連携（20〜22年度）」　東海4県11大学連携　東海臨床薬学連携センター長
    年月日（From)
    2008/10
    年月日（To）
    2013/03
    概要
    平成20年度から、愛知、岐阜、三重、静岡の11大学の連携において、東海臨床薬学連携センター長として、申請、運営、取りまとめを行った。平成18年度から始まった6年制薬学教育を実施していくために、5つの実施部会を組織し活動を行った。

実務経験を有する者についての特記事項（教育上の能力）

 1
  • 件名
    東京大学医学部附属病院分院薬剤部長
    年月日（From)
    2003/10
    年月日（To）
    2006/04

資格・免許

 1
  • 件名
    薬剤師免許
    年月日
    1976/06/12

実務経験を有する者についての特記事項（職務上の実績）

 1
  • 件名
    東京大学医学部附属病院 分院薬剤部長
    年月日（From)
    1993/10/16
    年月日（To)
    1996/04/25
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