Curriculum Vitaes

ONO HIDEKI

  (小野 秀樹)

Profile Information

Affiliation
Faculty of Pharmacy Department of Pharmaceutical Sciences, Musashino University
Degree
薬学博士(東京大学)

J-GLOBAL ID
200901084214854756
researchmap Member ID
1000212505

Research History

 11

Papers

 169
  • Akihiro Fukushima, Arisa Fukui, Yuki Takemura, Yasuhiro Maeda, Hideki Ono
    Journal of pharmacological sciences, 136(1) 39-41, Jan, 2018  
    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), Dec 1, 2017  
    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, Feb, 2017  Peer-reviewed
    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.
  • Shohei Yamamoto, Yuma Suzuki, Hideki Ono, Kazuhiko Kume, Masahiro Ohsawa
    EUROPEAN JOURNAL OF PHARMACOLOGY, 793 66-75, Dec, 2016  Peer-reviewed
    Cilnidipine is a dihydropyridine derivative that inhibits N-type and L-type voltage-gated Ca2+ channels (VDCCs). We recently reported that a selective N-type VDCC blocker attenuated the spinal long-term potentiation (LTP) of C-fiber-evoked field potentials recorded in the spinal dorsal horn of rats, which served as a model for examining synaptic function during central pain sensitization. In this study, we investigated the effects of cilnidipine on the changes related to neuropathic pain induced by nerve injury. Mechanical allodynia and hyperalgesia were evaluated by von Frey test and pin prick test, respectively. Spinal LTP of C-fiber-evoked field potentials were evaluated by in vivo electrophysiology. Intrathecally administrated cilnidipine attenuated mechanical allodynia and hyperalgesia in the spared nerve injury mouse model. Using in vivo electrophysiology in rats, cilnidipine (10 mu m) administered spinally inhibited the induction and maintenance of high-frequency stimulation-induced LTP of C-fiber-evoked field potentials, while basal C-fiber-evoked field potentials in naive rats were unaffected. The basal C-fiber-evoked field potentials in nerve-injured rats were strongly inhibited by cilnidipine. Treatment with a specific N-type VDCC blocker, omega o-conotoxin GVIA, which reportedly attenuates C-fiber-evoked field potentials both before and after the induction of LTP, attenuated mechanical allodynia and hyperalgesia in nerve-injured mice. By contrast, an L-type VDCC blocker, nicardipine attenuated only mechanical hyperalgesia, but not mechanical allodynia in nerve-injured mice, and also attenuated the established LTP of C-fiber-evoked field potentials in rats. These results suggested that N-type and L-type VDCC blockers may effectively alleviate the hyperalgesia and allodynia associated with neuropathic pain without affecting normal pain perception.
  • Shohei Yamamoto, Hideki Ono, Kazuhiko Kume, Masahiro Ohsawa
    JOURNAL OF PHARMACOLOGICAL SCIENCES, 130(4) 189-193, Apr, 2016  Peer-reviewed
    Oxaliplatin (L-OHP) is a platinum-based chemotherapy drug, used in standard treatment of colorectal cancer. L-OHP frequently causes acute peripheral neuropathies. These adverse effects limit cancer therapy with L-OHP. The present study was designed to reveal the changes in sensory nerve function in L-OHP-injected rats. Mechanical static allodynia, dynamic allodynia, and cold allodynia were evaluated using the von Frey test, brush test, and acetone test, respectively. Sensory nerve fiber responsiveness was measured using a Neurometer. The fifth lumbar ventral root was sectioned to record multi-unit efferent discharges. Single intraperitoneal administration of L-OHP induced mechanical static allodynia, dynamic allodynia, and cold allodynia in Wistar/ST rats. The thresholds for paw withdrawal induced by 2000 Hz (A beta-fiber) and 5 Hz (C-fiber), but not 250 Hz (A delta-fiber) sine-wave electrical stimulation were reduced in L-OHP-treated rats. Multi-unit efferent discharges were increased by mechanical stimulation using a von Frey filament applied to the plantar surface of the hindpaw. The discharges during and after stimulation were increased in the L-OHP-treated rats. Cold stimulation, but not brush stimulation, increased the discharges in L-OHP-treated rats. These results suggest that sensitization of A beta- and C-fibers, but not A delta-fibers, contributes to the development of L-OHP-induced mechanical and cold allodynia. (C) 2015 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society. This is an open access article under the CC BY-NC-ND license.

Misc.

 93
  • Masahiro Ohsawa, Shohei Yamamoto, Hideki Ono
    YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN, 134(3) 387-395, Mar, 2014  
    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, Jul, 2013  
  • Yu Masegi, Hideki Ono, Mitsuo Tanabe
    JOURNAL OF PHARMACOLOGICAL SCIENCES, 118 194P-194P, 2012  
  • Seiya Kuraoka, Hideki Ono, Mitsuo Tanabe
    JOURNAL OF PHARMACOLOGICAL SCIENCES, 118 193P-193P, 2012  
  • Saki Otake, Shohei Yamamoto, Masahiro Ohsawa, Masahide Noji, Hideki Ono
    JOURNAL OF PHARMACOLOGICAL SCIENCES, 118 146P-146P, 2012  

Books and Other Publications

 32

Presentations

 21

Research Projects

 20

教育内容・方法の工夫

 2
  • Subject
    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
    Date(From)
    2005/12
    Date(To)
    2008
    Summary
    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。
  • Subject
    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
    Date(From)
    2008/10
    Date(To)
    2013/03
    Summary
    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
  • Subject
    東京大学医学部附属病院分院薬剤部長
    Date(From)
    2003/10
    Date(To)
    2006/04

資格・免許

 1
  • Subject
    薬剤師免許
    Date
    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
  • Subject
    東京大学医学部附属病院 分院薬剤部長
    Date(From)
    1993/10/16
    Date(To)
    1996/04/25