CVClient

Yamamoto Shohei

  (山本 昇平)

Profile Information

Affiliation
助教, 薬学部 薬学科, 武蔵野大学
Degree
博士 (薬学)(名古屋市立大学大学院 薬学研究科)

J-GLOBAL ID
201701018192179510
researchmap Member ID
B000269635

Research History

 5

Committee Memberships

 1

Papers

 20
  • Tatsuhiro Akaishi, Shohei Yamamoto, Kazuho Abe
    Biological and Pharmaceutical Bulletin, 46(7) 914-920, Jul 1, 2023  Peer-reviewedLead author
  • Tatsuhiro Akaishi, Shohei Yamamoto, Kazuho Abe
    Biological and Pharmaceutical Bulletin, 45(3) 301-308, Mar 1, 2022  Peer-reviewedLead author
  • Tatsuhiro Akaishi, Shohei Yamamoto, Kazuho Abe
    Biological & pharmaceutical bulletin, 43(1) 138-144, 2020  Peer-reviewed
    We have recently found that the synthetic curcumin derivative CNB-001 suppresses lipopolysaccharide (LPS)-induced nitric oxide (NO) production in cultured microglia, demonstrating that it exerts anti-neuroinflammatory effects by regulating microglial activation. To explore the molecular mechanisms underlying the anti-inflammatory effect of CNB-001, the present study investigated whether CNB-001 is also effective for microglial NO production induced by other stimulants than LPS. Treatment of primary cultured rat microglia with thrombin, a serine protease that has been proposed as a mediator of cerebrovascular injuries, caused the expression of inducible NO synthase (iNOS) and the production of NO. The thrombin-induced NO production was completely blocked by the presence of SCH-79797, a selective protease-activated receptor 1 (PAR-1) antagonist, suggesting that the effect of thrombin is mediated by PAR-1. CNB-001 (1-10 µM) attenuated the thrombin-induced iNOS expression and NO production without affecting the PAR-1 expression. In addition, thrombin treatment caused rapid phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK). The changes in ERK and p38 MAPK were significantly suppressed by the presence of CNB-001. These results demonstrate that CNB-001 suppresses thrombin-stimulated microglial activation by inhibiting the ERK and p38 MAPK pathways.
  • Shohei Yamamoto, Yuma Suzuki, Hideki Ono, Kazuhiko Kume, Masahiro Ohsawa
    EUROPEAN JOURNAL OF PHARMACOLOGY, 793 66-75, Dec, 2016  Peer-reviewedLead author
    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-reviewedLead author
    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.

 20
  • 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  
  • Saki Otake, Shohei Yamamoto, Masahiro Ohsawa, Masahide Noji, Hideki Ono
    JOURNAL OF PHARMACOLOGICAL SCIENCES, 118 146P-146P, 2012  
  • Yui Iwajima, Yuko Nagano, Shohei Yamamoto, Yasuhiro Maeda, Masahiro Ohsawa, Hideki Ono
    JOURNAL OF PHARMACOLOGICAL SCIENCES, 118 153P-153P, 2012  
  • Yuma Suzuki, Shohei Yamamoto, Masahiro Ohsawa, Hideki Ono
    JOURNAL OF PHARMACOLOGICAL SCIENCES, 118 146P-146P, 2012  

Research Projects

 2

資格・免許

 1
  • Subject
    薬剤師免許
    Date
    2002/06