Details of the Researcher

PHOTO

Minoru Wakamori
Section
Graduate School of Dentistry
Job title
Professor
Degree

  • (BLANK) (Tohoku University)

Research History 10

  • 2020/04 - Present
    Tohoku University　Graduate School of Dentistry　Professor

  • 2007/04 - 2020/03
    Tohoku University　Graduate School of Dentistry

  • 2004/04 - 2007/03
    Kyoto University　Graduate School of Engineering, Department of Synthetic Chemistry and Biological Chemistry

  • 2002/04 - 2005/03
    岡崎国立共同研究機構　生理学研究所 生体情報研究系 情報記憶研究部門（客員部門）　客員准教授

  • 2003/04 - 2004/03
    Kagoshima University　Graduate School of Medical and Dental Sciences

  • 2001/03 - 2003/03
    Kagoshima University　Faculty of Medicine, Department of Medicine

  • 1995/12 - 2001/02
    岡崎国立共同研究機構　生理学研究所 生体情報研究系 液性情報研究部門　助手

  • 1995/04 - 1995/11
    オハイオ州立シンシナティ大学　医学部分子薬理学及び生物物理学研究所　助手

  • 1994/07 - 1995/03
    オハイオ州立シンシナティ大学　医学部分子薬理学及び生物物理学研究所　博士研究員

  • 1992/04 - 1994/06
    オハイオ州立シンシナティ大学　医学部薬理学及び細胞生物物理学講座　博士研究員

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Professional Memberships 4

  • JAPANESE DENTAL EDUCATION ASSOCIATION

  • 北米神経科学会

  • JAPANESE ASSOCIATION FOR ORAL BIOLOGY

  • THE JAPANESE PHARMACOLOGICAL SOCIETY

Research Interests 8

  • 歯科薬理学

  • 分子薬理学

  • 口腔生理学

  • 神経生理学

  • 分子細胞生理学

  • Orofacial physiology

  • Neurophysiology

  • Molecular & Cellular Physiology

Research Areas 4

  • Life sciences / Oral medicine /

  • Life sciences / Clinical pharmacy /

  • Life sciences / Physiology /

  • Life sciences / Neuroscience - general /

Papers 69

  1. Molecular mechanism for transcriptional regulation of the parathyroid hormone gene by Epiprofin. International-journal

    Takashi Nakamura, Hannah M Nakamura, Yasumasa Iwasaki, Motomi Enomoto-Iwamoto, Noriaki Nakashima, Satoshi Fukumoto, Maurizio Pacifici, Masahiro Iwamoto, Minoru Wakamori

    The FEBS journal　2025/03/31

    DOI： 10.1111/febs.70085 　

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    Epiprofin (Epfn), an Sp/KLF family transcription factor that regulates cell proliferation and determines cell fates, is essential for normal skin, hair follicle, and tooth development. We found that Epfn was expressed in parathyroid glands, and Epfn-knockout mice displayed elevated serum parathyroid hormone (PTH) concentrations, decreased bone volume, and intracranial ectopic calcification. To investigate the role of Epfn in the regulation of PTH expression, parathyroid gland explant and parathyroid cell line culture methods were used. Epfn expression was found to be upregulated in response to an increase in extracellular calcium concentration, whereas PTH expression was downregulated, thus demonstrating an inverse correlation. Forced expression of Epfn inhibited PTH gene expression and PTH promoter reporter activity in parathyroid cells. In addition, with a high extracellular calcium concentration, Epfn silencing in cultured parathyroid glands failed to block PTH gene expression. ChIP-qPCR analysis also revealed Epfn binding in the proximal region of the PTH promoter, which was accelerated in the presence of a high concentration of calcium ions. The results from our in vitro and ex vivo analyses suggest that Epfn is a newly identified negative regulator of PTH transcription by regulating the proximal PTH promoter. Furthermore, the expression of Epfn was significantly reduced in parathyroid adenomas of primary hyperparathyroidism patients. The identification of Epfn as a potential therapeutic target for the control of PTH production in hyperparathyroidism patients opens new avenues for targeted treatment approaches.

  2. Periodontal Ligaments Enhance Neurite Outgrowth in Trigeminal Ganglion Neurons through Wnt5a Production Induced by Mechanical Stimulation Peer-reviewed

    Kaori Takahashi, Takashi Yoshida, Minoru Wakamori

    American Journal of Physiology-Cell Physiology　323　(6)　C1704-C1719　2022/11/14

    Publisher: American Physiological Society

    DOI： 10.1152/ajpcell.00302.2022 　

    ISSN： 0363-6143

    eISSN： 1522-1563

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    The peripheral sensory nerve must be maintained to perceive environmental changes. Daily physiological mechanical stimulations, like gravity, floor reaction force and occlusal force, influence the nerve homeostasis directly or indirectly. Although the direct axonal membrane stretch enhances axon outgrowth via mechanosensitive channel activation, the indirect mechanisms remain to be elucidated. In this study, we identified the indirect pathways where Wnt5a was a molecular cue released by mechanically stimulated rat periodontal ligament (rPDL) cells. qRT-PCR and ELISA showed that mechanically stimulated rPDL cells enhanced Wnt5a expression level and Wnt5a protein in a Ca2+-dependent manner. The inhibitors of PI3K (LY294002) and MEK1/2 (U0126) suppressed the Akt/PKB and ERK1/2 phosphorylation, respectively, in western blotting analysis and consequently abolished the increase in Wnt5a expression. Similarly, PF573228, a focal adhesion kinase inhibitor, attenuated Akt- and ERK1/2-phosphorylation and Wnt5a expression. Importantly, the culture medium of stretched PDL cells enhanced neurite elongation, sprouting, and branching in trigeminal ganglion neurons which project to PDL. Moreover, treatment with an anti-Wnt5a antibody (to neutralize Wnt5a activity), AP7677a (anti-Ryk antibody, to block Ryk receptor activity), or strictinin (Ror1 inhibitor) suppressed the morphological changes. These findings reveal the indirect mechanisms that Wnt5a, released from the connective tissues in response to mechanical stimulation, enhances the outgrowth of the peripheral nerves. Our study suggests that the peripheral connective tissues regulate peripheral nerve homeostasis and that Wnt5a signaling could be targeted for the treatment of peripheral nerve disorders.

  3. 副交感神経から分泌されるアセチルコリン(ACh)が、唾液腺の発生過程で筋上皮細胞の分化誘導と機能的器官内配置を決定している(Acetylcholine(ACh), a parasympathetic neurotransmitter, orchestrates the induction and the positioning of myoepithelial cells in developing salivary glands)

    真藤 裕基, 若森 実, 中井 淳一, 中村 卓史

    Journal of Oral Biosciences Supplement　2022　250-250　2022/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  4. A parasympathetic neurotransmitter induces myoepithelial cell differentiation during salivary gland development Peer-reviewed

    Yuki Shindo, Hannah M. Nakamura, Junichi Nakai, Minoru Wakamori, Takashi Nakamura

    Experimental Cell Research　416　(1)　113137-113137　2022/07

    Publisher: Elsevier BV

    DOI： 10.1016/j.yexcr.2022.113137 　

    ISSN： 0014-4827

  5. Identification of ultra-rare disruptive variants in voltage-gated calcium channel-encoding genes in Japanese samples of schizophrenia and autism spectrum disorder International-journal Peer-reviewed

    Chenyao Wang, Shin-ichiro Horigane, Minoru Wakamori, Shuhei Ueda, Takeshi Kawabata, Hajime Fujii, Itaru Kushima, Hiroki Kimura, Kanako Ishizuka, Yukako Nakamura, Yoshimi Iwayama, Masashi Ikeda, Nakao Iwata, Takashi Okada, Branko Aleksic, Daisuke Mori, Takashi Yoshida, Haruhiko Bito, Takeo Yoshikawa, Sayaka Takemoto-Kimura, Norio Ozaki

    Translational Psychiatry　12　(1)　84-84　2022/02

    Publisher: Springer Science and Business Media LLC

    DOI： 10.1038/s41398-022-01851-y 　

    eISSN： 2158-3188

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    Abstract Several large-scale whole-exome sequencing studies in patients with schizophrenia (SCZ) and autism spectrum disorder (ASD) have identified rare variants with modest or strong effect size as genetic risk factors. Dysregulation of cellular calcium homeostasis might be involved in SCZ/ASD pathogenesis, and genes encoding L-type voltage-gated calcium channel (VGCC) subunits Cav1.1 (CACNA1S), Cav1.2 (CACNA1C), Cav1.3 (CACNA1D), and T-type VGCC subunit Cav3.3 (CACNA1I) recently were identified as risk loci for psychiatric disorders. We performed a screening study, using the Ion Torrent Personal Genome Machine (PGM), of exon regions of these four candidate genes (CACNA1C, CACNA1D, CACNA1S, CACNA1I) in 370 Japanese patients with SCZ and 192 with ASD. Variant filtering was applied to identify biologically relevant mutations that were not registered in the dbSNP database or that have a minor allele frequency of less than 1% in East-Asian samples from databases; and are potentially disruptive, including nonsense, frameshift, canonical splicing site single nucleotide variants (SNVs), and non-synonymous SNVs predicted as damaging by five different in silico analyses. Each of these filtered mutations were confirmed by Sanger sequencing. If parental samples were available, segregation analysis was employed for measuring the inheritance pattern. Using our filter, we discovered one nonsense SNV (p.C1451* in CACNA1D), one de novo SNV (p.A36V in CACNA1C), one rare short deletion (p.E1675del in CACNA1D), and 14 NSstrict SNVs (non-synonymous SNV predicted as damaging by all of five in silico analyses). Neither p.A36V in CACNA1C nor p.C1451* in CACNA1D were found in 1871 SCZ cases, 380 ASD cases, or 1916 healthy controls in the independent sample set, suggesting that these SNVs might be ultra-rare SNVs in the Japanese population. The neuronal splicing isoform of Cav1.2 with the p.A36V mutation, discovered in the present study, showed reduced Ca2+-dependent inhibition, resulting in excessive Ca2+ entry through the mutant channel. These results suggested that this de novo SNV in CACNA1C might predispose to SCZ by affecting Ca2+ homeostasis. Thus, our analysis successfully identified several ultra-rare and potentially disruptive gene variants, lending partial support to the hypothesis that VGCC-encoding genes may contribute to the risk of SCZ/ASD.

  6. Mode-selective inhibitory effects of eugenol on the mouse TRPV1 channel. International-journal Peer-reviewed

    Kaori Takahashi, Takashi Yoshida, Minoru Wakamori

    Biochemical and biophysical research communications　556　156-162　2021/06/04

    DOI： 10.1016/j.bbrc.2021.03.126 　

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    The transient receptor potential vanilloid 1 (TRPV1) channel is a polymodal receptor in sensory nerves and involved in pain sensation. TRPV1 has at least three distinct activation modes that are selectively induced by different stimuli capsaicin, noxious heat, and protons. Although many mode-selective TRPV1 antagonists have been developed for their anticipated analgesic effects, there have been few successful reports because of adverse effects due to burn injuries and hyperthermia. Eugenol is a vanilloid that has been used as an analgesic in the dental treatment, and its TRPV1 activation ability has been reported. However, our knowledge about the underlying mechanisms of the antagonistic effects of eugenol on TRPV1 activation induced by three different modes is limited. Here, we show that eugenol dose-dependently inhibited the capsaicin-activated inward currents of mouse TRPV1 expressed in human embryonic kidney 293 (HEK293) cells. Under low pH conditions, low concentrations of eugenol only enhanced the proton-induced TRPV1 currents, whereas high eugenol concentrations initially potentiated but then immediately abrogated TRPV1 currents. Finally, eugenol had no modulatory effects on heat-activated TRPV1 in electrophysiological and Fura-2-based Ca2+ imaging experiments. Our results demonstrate that eugenol is a mode-selective antagonist of TRPV1 and can be evaluated as a lead compound of analgesics targeting TRPV1 without serious side effects.

  7. Capsaicin and Proton Differently Modulate Activation Kinetics of Mouse Transient Receptor Potential Vanilloid-1 Channel Induced by Depolarization. International-journal Peer-reviewed

    Kaori Takahashi, Kentaro Araki, Hideo Miyamoto, Rikimaru Shirakawa, Takashi Yoshida, Minoru Wakamori

    Frontiers in pharmacology　12　672157-672157　2021

    DOI： 10.3389/fphar.2021.672157 　

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    The transient receptor potential vanilloid type 1 (TRPV1) channel is a non-selective cation channel expressed with transient receptor potential ankyrin type 1 (TRPA1) in small and medial size neurons of the dorsal root ganglions and trigeminal ganglions. TRPV1 is activated by capsaicin, thermal stimuli higher than 43°C, mechanical stress, and protons (H+). Although the TRPV1 channel does not have positively charged residues at regular intervals on its transmembrane segments, alterations in membrane potential also affect the state of TRPV1 channel. In the presence of capsaicin, voltage-dependent probability of opening of the TRPV1 channel and its kinetics have been examined, but the characteristics in the low pH remain unclear. To understand the voltage-dependency of the TRPV1 channel activation, we recorded capsaicin- and proton-induced mouse TRPV1 channel currents in a heterologous expression system. Outward current evoked by depolarizing square pulses in the presence of capsaicin or protons was fitted to a two-exponential function with a time-independent component. The voltage-dependent changes in amplitude of the three components displayed shallow curves and the changes in their ratio to the total current display similar tendencies in the presence of capsaicin and under the low pH. However, the fast and slow time constants in the presence of capsaicin were respectively 5- and 8-fold lower than those obtained under low pH conditions. These results suggest that the TRPV1 channel slowly drives the feed-forward cycle of pain sensation, and capsaicin and protons differently modulate the voltage-dependent TRPV1 channel gating.

  8. Paeonol, an Ingredient of Kamishoyosan, Reduces Intracellular Lipid Accumulation by Inhibiting Glucocorticoid Receptor Activity in 3T3-L1 Cells Peer-reviewed

    Masayuki Izumi, Takashi Yoshida, Takashi Nakamura, Minoru Wakamori

    Nutrients　12　(2)　309-309　2020/01/24

    Publisher: MDPI AG

    DOI： 10.3390/nu12020309 　

    eISSN： 2072-6643

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    Excessive triglyceride accumulation in lipid-metabolizing tissues is associated with an increased risk of a variety of metabolic diseases. Kamishoyosan (KSS) is a Kampo composed of 10 constituent herbs, and contains moutan cortex (MC) and paeonol (PN) as the major ingredient of MC. Here, we demonstrate the molecular mechanism underlying the effect of KSS on the differentiation of mouse preadipocytes (3T3-L1 cells). KSS inhibited the accumulation of triglycerides in a dose-dependent manner in 3T3-L1 cells that were induced to differentiate into adipocytes. We also found that MC and PN were responsible for the anti-adipogenetic effect of KSS and significantly suppressed the expression of CCAAT/enhancer-binding proteins-δ (C/EBP-δ) mRNA 3 days after the induction of differentiation. Thus, PN may contribute to the anti-adipogenetic property of MC in 3T3-L1 cells. In addition, PN inhibited dexamethasone (Dex)-induced glucocorticoid receptor (GR) promoter activity. Taken together, these results suggest that PN suppresses C/EBP-δ expression by inhibiting Dex-induced GR promoter activity at the early stage of differentiation and, consequently, delays differentiation into mature adipocytes. Our results suggest that the habitual intake of Kampo-containing PN contributes to the prevention of the onset of metabolic diseases by decreasing the excessive accumulation of triglycerides in lipid-metabolizing tissues.

  9. Synthesis of quinolyl-pyrrole derivatives as novel environment-sensitive fluorescent probes Peer-reviewed

    Shinotsuka R, Oba T, Mitome T, Masuya T, Ito S, Murakami Y, Kagenishi T, Kodama Y, Matsuda M, Yoshida T, Wakamori M, Ohkura M, Nakai J

    Journal of Photochemistry and Photobiology A: Chemistry　382　111900-111900　2019

    Publisher: Elsevier BV

    DOI： 10.1016/j.jphotochem.2019.111900 　

    ISSN： 1010-6030

  10. Protective effects of duloxetine against cerebral ischemia-reperfusion injury via transient receptor potential melastatin 2 inhibition International-journal Peer-reviewed

    Toda T, Yamamoto S, Umehara N, Mori Y, Wakamori M, Shimizu S

    Journal of Pharmacology and Experimental Therapeutics　368　(2)　246-254　2019

    DOI： 10.1124/jpet.118.253922 　

  11. Differential binding of tetrodotoxin and its derivatives to voltage-sensitive sodium channel subtypes (Na(v)1.1 to Na(v)1.7) Peer-reviewed

    Tadaaki Tsukamoto, Yukie Chiba, Minoru Wakamori, Tomoshi Yamada, Shunsuke Tsunogae, Yuko Cho, Ryo Sakakibara, Takuya Imazu, Shouta Tokoro, Yoshiki Satake, Masaatsu Adachi, Toshio Nishikawa, Mari Yotsu-Yamashita, Keiichi Konoki

    BRITISH JOURNAL OF PHARMACOLOGY　174　(21)　3881-3892　2017/11

    DOI： 10.1111/bph.13985 　

    ISSN： 0007-1188

    eISSN： 1476-5381

  12. Alternative splicing in the C-terminal tail of Ca(v)2.1 is essential for preventing a neurological disease in mice Peer-reviewed

    Tomonori Aikawa, Takaki Watanabe, Taisuke Miyazaki, Takayasu Mikuni, Minoru Wakamori, Miyano Sakurai, Hidenori Aizawa, Nobutaka Ishizu, Masahiko Watanabe, Masanobu Kano, Hidehiro Mizusawa, Kei Watase

    HUMAN MOLECULAR GENETICS　26　(16)　3094-3104　2017/08

    DOI： 10.1093/hmg/ddx193 　

    ISSN： 0964-6906

    eISSN： 1460-2083

  13. Pharmacological properties of SAK3, a novel T-type voltage-gated Ca2+ channel enhancer Peer-reviewed

    Yasushi Yabuki, Kazuya Matsuo, Hisanao Izumi, Hidaka Haga, Takashi Yoshida, Minoru Wakamori, Akikazu Kakei, Kenji Sakimura, Takaichi Fukuda, Kohji Fukunaga

    NEUROPHARMACOLOGY　117　1-13　2017/05

    DOI： 10.1016/j.neuropharm.2017.01.011 　

    ISSN： 0028-3908

    eISSN： 1873-7064

  14. Inhibition of veratridine-induced delayed inactivation of the voltage-sensitive sodium channel by synthetic analogs of crambescin B Peer-reviewed

    Tadaaki Tsukamoto, Yukie Chiba, Atsuo Nakazaki, Yuki Ishikawa, Yoshiki Nakane, Yuko Cho, Mad Yotsu-Yamashita, Toshio Nishikawa, Minoru Wakamori, Keiichi Konoki

    BIOORGANIC & MEDICINAL CHEMISTRY LETTERS　27　(5)　1247-1251　2017/03

    DOI： 10.1016/j.bmcl.2017.01.054 　

    ISSN： 0960-894X

    eISSN： 1464-3405

  15. Unraveling the rat blood genome-wide transcriptome after oral administration of lavender oil by a two-color dye-swap DNA microarray approach Peer-reviewed

    Motohide Hori, Hiroko Kubo, Junko Shibato, Tomomi Saito, Tetsuo Ogawa, Minoru Wakamori, Yoshinori Masuo, Seiji Shioda, Randeep Rakwal

    Genomics Data　8　139-145　2016/06/01

    Publisher: Elsevier Inc

    DOI： 10.1016/j.gdata.2016.05.005 　

    ISSN： 2213-5960

  16. Compromised maturation of GABAergic inhibition underlies abnormal network activity in the hippocampus of epileptic Ca2+ channel mutant mice, tottering Peer-reviewed

    Akito Nakao, Takafumi Miki, Ken Shimono, Hiroaki Oka, Tomohiro Numata, Shigeki Kiyonaka, Kaori Matsushita, Hiroo Ogura, Tetsuhiro Niidome, Jeffrey L. Noebels, Minoru Wakamori, Keiji Imoto, Yasuo Mori

    PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY　467　(4)　737-752　2015/04

    DOI： 10.1007/s00424-014-1555-6 　

    ISSN： 0031-6768

    eISSN： 1432-2013

  17. Inhibitory effects of AG490 on H2O2-induced TRPM2-mediated Ca2+ entry Peer-reviewed

    Shunichi Shimizu, Ryo Yonezawa, Tamio Hagiwara, Takashi Yoshida, Nobuaki Takahashi, Satoshi Hamano, Takaharu Negoro, Takahiro Toda, Minoru Wakamori, Yasuo Mori, Masakazu Ishii

    EUROPEAN JOURNAL OF PHARMACOLOGY　742　22-30　2014/11

    DOI： 10.1016/j.ejphar.2014.08.023 　

    ISSN： 0014-2999

    eISSN： 1879-0712

  18. Development of Purkinje cell degeneration in a knockin mouse model reveals lysosomal involvement in the pathogenesis of SCA6 Peer-reviewed

    Toshinori Unno, Minoru Wakamori, Masato Koike, Yasuo Uchiyama, Kinya Ishikawa, Hisahiko Kubota, Takashi Yoshida, Hiroko Sasakawa, Christoph Peters, Hidehiro Mizusawa, Kei Watase

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA　109　(43)　17693-17698　2012/10

    DOI： 10.1073/pnas.1212786109 　

    ISSN： 0027-8424

  19. Inactivation of voltage-gated Ca2+ channels and cone-rod dystrophy CORD7

    Minoru Wakamori, Yoshitsugu Uriu, Takafumi Miki, Shigeki Kiyonaka, Yasuo Mori

    Hirosaki Medical Journal　61　S53-S62　2010/07/08

    ISSN： 0439-1721

  20. Rab3-interacting Molecule gamma Isoforms Lacking the Rab3-binding Domain Induce Long Lasting Currents but Block Neurotransmitter Vesicle Anchoring in Voltage-dependent P/Q-type Ca2+ Channels Peer-reviewed

    Yoshitsugu Uriu, Shigeki Kiyonaka, Takafumi Miki, Masakuni Yagi, Satoshi Akiyama, Emiko Mori, Akito Nakao, Aaron M. Beedle, Kevin P. Campbell, Minoru Wakamori, Yasuo Mori

    JOURNAL OF BIOLOGICAL CHEMISTRY　285　(28)　21750-21767　2010/07

    DOI： 10.1074/jbc.M110.101311 　

    ISSN： 0021-9258

  21. A Missense Mutation of the Gene Encoding Voltage-Dependent Sodium Channel (Na(v)1.1) Confers Susceptibility to Febrile Seizures in Rats Peer-reviewed

    Tomoji Mashimo, Iori Ohmori, Mamoru Ouchida, Yukihiro Ohno, Toshiko Tsurumi, Takafumi Miki, Minoru Wakamori, Shizuka Ishihara, Takashi Yoshida, Akiko Takizawa, Megumi Kato, Masumi Hirabayashi, Masashi Sasa, Yasuo Mori, Tadao Serikawa

    JOURNAL OF NEUROSCIENCE　30　(16)　5744-5753　2010/04

    DOI： 10.1523/JNEUROSCI.3360-09.2010 　

    ISSN： 0270-6474

  22. A Pathogenic C Terminus-truncated Polycystin-2 Mutant Enhances Receptor-activated Ca2+ Entry via Association with TRPC3 and TRPC7 Peer-reviewed

    Kyoko Miyagi, Shigeki Kiyonaka, Kazunori Yamada, Takafumi Miki, Emiko Mori, Kenta Kato, Tomohiro Numata, Yuichi Sawaguchi, Takuro Numaga, Toru Kimura, Yoshikatsu Kanai, Mitsuhiro Kawano, Minoru Wakamori, Hideki Nomura, Ichiro Koni, Masakazu Yamagishi, Yasuo Mori

    JOURNAL OF BIOLOGICAL CHEMISTRY　284　(49)　34400-34412　2009/12

    DOI： 10.1074/jbc.M109.015149 　

    ISSN： 0021-9258

  23. Knockdown of Ca(v)2.1 calcium channels is sufficient to induce neurological disorders observed in natural occurring Cacna1a mutants in mice Peer-reviewed

    Hiromitsu Saito, Motohiro Okada, Takafumi Miki, Minoru Wakamori, Akira Futatsugi, Yasuo Mori, Katsuhiko Mikoshiba, Noboru Suzuki

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　390　(3)　1029-1033　2009/12

    DOI： 10.1016/j.bbrc.2009.10.102 　

    ISSN： 0006-291X

  24. Selective and direct inhibition of TRPC3 channels underlies biological activities of a pyrazole compound Peer-reviewed

    Shigeki Kiyonaka, Kenta Kato, Motohiro Nishida, Kazuhiro Mio, Takuro Numaga, Yuichi Sawaguchi, Takashi Yoshida, Minoru Wakamori, Emiko Mori, Tomohiro Numata, Masakazu Ishii, Hiroki Takemoto, Akio Ojida, Kenta Watanabe, Aya Uemura, Hitoshi Kurose, Takashi Morii, Tsutomu Kobayashi, Yoji Sato, Chikara Sato, Itaru Hamachi, Yasuo Mori

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA　106　(13)　5400-5405　2009/03

    DOI： 10.1073/pnas.0808793106 　

    ISSN： 0027-8424

  25. Two novel alleles of tottering with distinct Ca(v)2.1 calcium channel neuropathologies Peer-reviewed

    T. Miki, T. A. Zwingman, M. Wakamori, C. M. Lutz, S. A. Cook, D. A. Hosford, K. Herrup, C. F. Fletcher, Y. Mori, W. N. Frankel, V. A. Letts

    NEUROSCIENCE　155　(1)　31-44　2008/07

    DOI： 10.1016/j.neuroscience.2008.05.028 　

    ISSN： 0306-4522

  26. Solution structure of agelenin, an insecticidal peptide isolated from the spider Agelena opulenta, and its structural similarities to insect-specific calcium channel inhibitors Peer-reviewed

    Nahoko Yamaji, Kenji Sugase, Terumi Nakajima, Takafumi Miki, Minoru Wakamori, Yasuo Mori, Takashi Iwashita

    FEBS LETTERS　581　(20)　3789-3794　2007/08

    DOI： 10.1016/j.febslet.2007.06.077 　

    ISSN： 0014-5793

  27. RIM1 confers sustained activity and neurotransmitter vesicle anchring to presynaptic Ca+2 channels Peer-reviewed

    Shigeki Kiyonaka, Minoru Wakamori, Takafumi Miki, Yoshitsugu Uriu, Mio Nonaka, Haruhiko Bito, Aaron M. Beedle, Emiko Mori, Yuji Hara, Michel De Waard, Motoi Kanagawa, Makoto Itakura, Masami Takahashi, Kevin P. Campbell, Yasuo Mori

    NATURE NEUROSCIENCE　10　(6)　691-701　2007/06

    DOI： 10.1038/nn1904 　

    ISSN： 1097-6256

  28. Mutation associated with an autosomal dominant cone-rod dystrophy CORD7 modifies RIM1-mediated modulation of voltage-dependent Ca2+ channels. Peer-reviewed

    Miki T, Kiyonaka S, Uriu Y, De Waard M, Wakamori M, Beedle AM, Campbell KP, Mori Y

    Channels (Austin, Tex.)　1　(3)　144-147　2007/05

    ISSN： 1933-6950

  29. Properties of human Ca(v)2.1 channel with a spinocerebellar ataxia type 6 mutation expressed in Purkinje cells Peer-reviewed

    Hironao Saegusa, Minoru Wakamori, Yoshihiro Matsuda, Junyang Wang, Yasuo Mori, Shuqin Zong, Tsutomu Tanabe

    MOLECULAR AND CELLULAR NEUROSCIENCE　34　(2)　261-270　2007/02

    DOI： 10.1016/j.mcn.2006.11.006 　

    ISSN： 1044-7431

  30. Mutation associated with an autosomal dominant cone-rod dystrophy CORD7 modifies RIM1-mediated modulation of voltage-dependent Ca2+ channels.

    Takafumi Miki, Shigeki Kiyonaka, Yoshitsugu Uriu, Michel De Waard, Minoru Wakamori, Aaron M Beedle, Kevin P Campbell, Yasuo Mori

    Channels (Austin, Tex.)　1　(3)　144-147　2007

    DOI： 10.4161/chan.4660 　

    ISSN： 1933-6969

  31. TRPC7 Peer-reviewed

    T. Numaga, M. Wakamori, Y. Mori

    Handbook of Experimental Pharmacology　179　(179)　143-151　2007

    DOI： 10.1007/978-3-540-34891-7_8 　

    ISSN： 0171-2004 1865-0325

  32. A Ca(V)2.1 calcium channel mutation rocker reduces the number of postsynaptic AMPA receptors in parallel fiber-Purkinje cell synapses Peer-reviewed

    Takashi Kodama, Yuko Itsukaichi-Nishida, Yugo Fukazawa, Minoru Wakamori, Mariko Miyata, Elek Molnar, Yasuo Mori, Ryuichi Shigemoto, Keiji Imoto

    EUROPEAN JOURNAL OF NEUROSCIENCE　24　(11)　2993-3007　2006/12

    DOI： 10.1111/j.1460-9568.2006.05191.x 　

    ISSN： 0953-816X

  33. Coupling of STIM1 to store-operated Ca2+ entry through its constitutive and inducible movement in the endoplasmic reticulum Peer-reviewed

    Yoshihiro Baba, Kenji Hayashit, Yoko Fujii, Akiko Mizushima, Hiroshi Watarai, Minoru Wakamori, Takuro Numaga, Yasuo Mori, Masamitsu Iino, Masaki Hikida, Tomohiro Kurosaki

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA　103　(45)　16704-16709　2006/11

    DOI： 10.1073/pnas.0608358103 　

    ISSN： 0027-8424

  34. Arachidonic acid can function as a signaling modulator by activating the TRPM5 cation channel in taste receptor cells Peer-reviewed

    Hideaki Oike, Minoru Wakamori, Yasuo Mori, Hiroki Nakanishi, Ryo Taguchi, Takumi Misaka, Ichiro Matsumoto, Keiko Abe

    BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS　1761　(9)　1078-1084　2006/09

    DOI： 10.1016/j.bbalip.2006.07.005 　

    ISSN： 1388-1981

    eISSN： 1879-2618

  35. A critical role of TRPM2 in neuronal cell death hy hydrogen peroxide Peer-reviewed

    S Kaneko, S Kawakami, Y Hara, M Wakamori, E Itoh, T Minami, Y Takada, T Kume, H Katsuki, Y Mori, A Akaike

    JOURNAL OF PHARMACOLOGICAL SCIENCES　101　(1)　66-76　2006/05

    DOI： 10.1254/jphs.FP0060128 　

    ISSN： 1347-8613

  36. A functional AMPA receptor-calcium channel complex in the postsynaptic membrane Peer-reviewed

    MG Kang, CC Chen, M Wakamori, Y Hara, Y Mori, KP Campbell

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA　103　(14)　5561-5566　2006/04

    DOI： 10.1073/pnas.0601289103 　

    ISSN： 0027-8424

  37. Ca2+-calmodulin-dependent myosin light chain kinase is essential for activation of TRPC5 channels expressed in HEK293 cells Peer-reviewed

    S Shimizu, T Yoshida, M Wakamori, M Ishii, T Okada, M Takahashi, M Seto, K Sakurada, Y Kiuchi, Y Mori

    JOURNAL OF PHYSIOLOGY-LONDON　570　(2)　219-235　2006/01

    DOI： 10.1113/jphysiol.2005.097998 　

    ISSN： 0022-3751

  38. Nicotinic ACh receptors in area postrema neurons of immature rat brain Peer-reviewed

    M Sorimachi, M Wakamori

    NEUROSCIENCE LETTERS　381　(3)　350-353　2005/06

    DOI： 10.1016/j.neulet.2005.02.052 　

    ISSN： 0304-3940

  39. Properties of native P2X receptors in large multipolar neurons dissociated from rat hypothalamic arcuate nucleus Peer-reviewed

    M Wakamori, M Sorimachi

    BRAIN RESEARCH　1005　(1-2)　51-59　2004/04

    DOI： 10.1016/j.brainres.2004.01.033 　

    ISSN： 0006-8993

  40. Bidirectional alterations in cerebellar synaptic transmission of tottering and rolling Ca2+ channel mutant mice Peer-reviewed

    K Matsushita, M Wakamori, IJ Rhyu, T Arii, S Oda, Y Mori, K Imoto

    JOURNAL OF NEUROSCIENCE　22　(11)　4388-4398　2002/06

    ISSN： 0270-6474

  41. Inhibitory effects of cilnidipine on peripheral and brain N-type Ca2+ channels expressed in BHK cells Peer-reviewed

    K Kato, M Wakamori, Y Mori, K Imoto, K Kitamura

    NEUROPHARMACOLOGY　42　(8)　1099-1108　2002/06

    DOI： 10.1016/S0028-3908(02)00053-9 　

    ISSN： 0028-3908

  42. Limited intercellular spread of spontaneous Ca2+ signals via gap junctions between mouse chromaffin cells in situ Peer-reviewed

    K Yamagami, T Moritoyo, M Wakamori, M Sorimachi

    NEUROSCIENCE LETTERS　323　(2)　97-100　2002/04

    DOI： 10.1016/S0304-3940(01)02578-2 　

    ISSN： 0304-3940

  43. Transient receptor potential 1 regulates capacitative Ca2+ entry and Ca2+ release from endoplasmic reticulum in B lymphocytes Peer-reviewed

    Y Mori, M Wakamori, T Miyakawa, M Hermosura, Y Hara, M Nishida, K Hirose, A Mizushima, M Kurosaki, E Mori, K Gotoh, T Okada, A Fleig, R Penner, M Iino, T Kurosaki

    JOURNAL OF EXPERIMENTAL MEDICINE　195　(6)　673-681　2002/03

    DOI： 10.1084/jem.20011758 　

    ISSN： 0022-1007

  44. LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death Peer-reviewed

    Y Hara, M Wakamori, M Ishii, E Maeno, M Nishida, T Yoshida, H Yamada, S Shimizu, E Mori, J Kudoh, N Shimizu, H Kurose, Y Okada, K Imoto, Y Mori

    MOLECULAR CELL　9　(1)　163-173　2002/01

    DOI： 10.1016/S1097-2765(01)00438-5 　

    ISSN： 1097-2765

  45. Differential nociceptive responses in mice lacking the alpha(IB) subunit of N-type Ca2+ channels Peer-reviewed

    S Hatakeyama, M Wakamori, M Ino, N Miyamoto, E Takahashi, T Yoshinaga, K Sawada, K Imoto, Tanaka, I, T Yoshizawa, Y Nishizawa, Y Mori, T Niidome, S Shoji

    NEUROREPORT　12　(11)　2423-2427　2001/08

    ISSN： 0959-4965

  46. The lethal expression of the GluR2flip/GluR4flip AMPA receptor in HEK293 cells Peer-reviewed

    M Iizuka, S Nishimura, M Wakamori, Akiba, I, K Imoto, EL Barsoumian

    EUROPEAN JOURNAL OF NEUROSCIENCE　12　(11)　3900-3908　2000/11

    DOI： 10.1046/j.1460-9568.2000.00270.x 　

    ISSN： 0953-816X

  47. Reduced voltage sensitivity of activation of P/Q-type Ca2+ channels is associated with the ataxic mouse mutation rolling Nagoya (tg(rol)) Peer-reviewed

    Y Mori, M Wakamori, S Oda, CF Fletcher, N Sekiguchi, E Mori, NG Copeland, NA Jenkins, K Matsushita, Z Matsuyama, K Imoto

    JOURNAL OF NEUROSCIENCE　20　(15)　5654-5662　2000/08

    ISSN： 0270-6474

  48. Spontaneous single-channel activity of neuronal TRP5 channel recombinantly expressed in HEK293 cells Peer-reviewed

    H Yamada, M Wakamori, Y Hara, Y Takahashi, K Konishi, K Imoto, Y Mori

    NEUROSCIENCE LETTERS　285　(2)　111-114　2000/05

    DOI： 10.1016/S0304-3940(00)01033-8 　

    ISSN： 0304-3940

  49. Stable expression of human homomeric and heteromeric AMPA receptor subunits in HEK293 cells Peer-reviewed

    S Nishimura, M Iizuka, M Wakamori, Akiba, I, K Imoto, EL Barsoumian

    RECEPTORS & CHANNELS　7　(2)　139-150　2000

    ISSN： 1060-6823

  50. Auxiliary subunits operate as a molecular switch in determining gating behaviour of the unitary N-type Ca2+ channel current in Xenopus oocytes Peer-reviewed

    M Wakamori, G Mikala, Y Mori

    JOURNAL OF PHYSIOLOGY-LONDON　517　(3)　659-672　1999/06

    DOI： 10.1111/j.1469-7793.1999.0659s.x 　

    ISSN： 0022-3751

  51. Direct alteration of the P/Q-type Ca2+ channel property by polyglutamine expansion in spinocerebellar ataxia 6. Peer-reviewed

    Matsuyama Z, Wakamori M, Mori Y, Kawakami H, Nakamura S, Imoto K

    The Journal of neuroscience　19　(12)　RC14　1999/06

    ISSN： 0270-6474

  52. Pharmacology of N-type Ca2+ channels distributed in cardiovascular system (Review) Peer-reviewed

    H Uneyama, A Takahara, M Wakamori, Y Mori, R Yoshimoto

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE　3　(5)　455-466　1999/05

    ISSN： 1107-3756

    eISSN： 1791-244X

  53. Halothane increases the open probability of glycine-activated channel current in rat central neurones Peer-reviewed

    M Wakamori, Y Ikemoto, M Yamashita

    BRITISH JOURNAL OF ANAESTHESIA　80　(6)　840-842　1998/06

    ISSN： 0007-0912

  54. Differential distribution of TRP Ca2+ channel isoforms in mouse brain Peer-reviewed

    Y Mori, N Takada, T Okada, M Wakamori, K Imoto, H Wanifuchi, H Oka, A Oba, K Ikenaka, T Kurosaki

    NEUROREPORT　9　(3)　507-515　1998/02

    ISSN： 0959-4965

  55. Functional characterization of ion permeation pathway in the N-type Ca2+ channel Peer-reviewed

    M Wakamori, M Strobeck, T Niidome, T Teramoto, K Imoto, Y Mori

    JOURNAL OF NEUROPHYSIOLOGY　79　(2)　622-634　1998/02

    DOI： 10.1152/jn.1998.79.2.622 　

    ISSN： 0022-3077

  56. STABLE EXPRESSION AND COUPLING OF CARDIAC L-TYPE CA2+ CHANNELS WITH BETA(1)-ADRENOCEPTORS Peer-reviewed

    A YATANI, M WAKAMORI, T NIIDOME, S YAMAMOTO, TANAKA, I, Y MORI, K KATAYAMA, S GREEN

    CIRCULATION RESEARCH　76　(3)　335-342　1995/03

    ISSN： 0009-7330

  57. DISTINCTIVE FUNCTIONAL-PROPERTIES OF THE NEURONAL BII (CLASS-E) CALCIUM-CHANNEL Peer-reviewed

    M WAKAMORI, T NIIDOME, D FURUTAMA, T FURUICHI, K MIKOSHIBA, Y FUJITA, TANAKA, I, K KATAYAMA, A YATANI, A SCHWARTZ, Y MORI

    RECEPTORS & CHANNELS　2　(4)　303-314　1994

    ISSN： 1060-6823

  58. BLOCK OF TRANSIENT OUTWARD-TYPE CLONED CARDIAC K+ CHANNEL CURRENTS BY QUINIDINE Peer-reviewed

    A YATANI, M WAKAMORI, G MIKALA, A BAHINSKI

    CIRCULATION RESEARCH　73　(2)　351-359　1993/08

    ISSN： 0009-7330

  59. HYPERPOLARIZING MUSCARINIC RESPONSES OF FRESHLY DISSOCIATED RAT HIPPOCAMPAL CA1 NEURONS Peer-reviewed

    M WAKAMORI, H HIDAKA, N AKAIKE

    JOURNAL OF PHYSIOLOGY-LONDON　463　585-604　1993/04

    ISSN： 0022-3751

  60. A NEW TYPE OF CA-2+ CHANNEL BLOCKER, NC-1100, INHIBITS THE LOW-THRESHOLD AND HIGH-THRESHOLD CA-2+ CURRENTS IN THE RAT CNS NEURONS Peer-reviewed

    N MIYAKE, M WAKAMORI, N AKAIKE

    BRAIN RESEARCH　598　(1-2)　215-220　1992/12

    ISSN： 0006-8993

  61. VOLTAGE-DEPENDENT CURRENTS IN ISOLATED SINGLE MERKEL CELLS OF RATS Peer-reviewed

    Y YAMASHITA, N AKAIKE, M WAKAMORI, IKEDA, I, H OGAWA

    JOURNAL OF PHYSIOLOGY-LONDON　450　143-162　1992/05

    ISSN： 0022-3751

  62. EFFECTS OF 2 VOLATILE ANESTHETICS AND A VOLATILE CONVULSANT ON THE EXCITATORY AND INHIBITORY AMINO-ACID RESPONSES IN DISSOCIATED CNS NEURONS OF THE RAT Peer-reviewed

    M WAKAMORI, Y IKEMOTO, N AKAIKE

    JOURNAL OF NEUROPHYSIOLOGY　66　(6)　2014-2021　1991/12

    DOI： 10.1152/jn.1991.66.6.2014 　

    ISSN： 0022-3077

  63. GAMMA-AMINOBUTYRIC ACID-INDUCED RESPONSE IN ACUTELY ISOLATED NUCLEUS-SOLITARII NEURONS OF THE RAT Peer-reviewed

    T NAKAGAWA, M WAKAMORI, T SHIRASAKI, T NAKAYE, N AKAIKE

    AMERICAN JOURNAL OF PHYSIOLOGY　260　(4)　C745-C749　1991/04

    DOI： 10.1152/ajpcell.1991.260.4.C745 　

    ISSN： 0002-9513

  64. DUAL EFFECT OF GLYCINE ON ISOLATED RAT SUPRACHIASMATIC NEURONS Peer-reviewed

    C ITO, M WAKAMORI, N AKAIKE

    AMERICAN JOURNAL OF PHYSIOLOGY　260　(2)　C213-C218　1991/02

    DOI： 10.1152/ajpcell.1991.260.2.C213 　

    ISSN： 0002-9513

  65. LOW-THRESHOLD CALCIUM CURRENT IN ISOLATED PURKINJE-CELL BODIES OF RAT CEREBELLUM Peer-reviewed

    M KANEDA, M WAKAMORI, C ITO, N AKAIKE

    JOURNAL OF NEUROPHYSIOLOGY　63　(5)　1046-1051　1990/05

    DOI： 10.1152/jn.1990.63.5.1046 　

    ISSN： 0022-3077

  66. GLYCINE-INSENSITIVE DESENSITIZATION OF N-METHYL-D-ASPARTATE RECEPTORS IN ACUTELY ISOLATED MAMMALIAN CENTRAL NEURONS Peer-reviewed

    T SHIRASAKI, T NAKAGAWA, M WAKAMORI, N TATEISHI, A FUKUDA, K MURASE, N AKAIKE

    NEUROSCIENCE LETTERS　108　(1-2)　93-98　1990/01

    ISSN： 0304-3940

  67. HIPPOCAMPAL CA1 PYRAMIDAL CELLS OF RATS HAVE 4 VOLTAGE-DEPENDENT CALCIUM CONDUCTANCES Peer-reviewed

    K TAKAHASHI, M WAKAMORI, N AKAIKE

    NEUROSCIENCE LETTERS　104　(1-2)　229-234　1989/09

    ISSN： 0304-3940

  68. EFFECTS OF CHLORDIAZEPOXIDE, CHLORPROMAZINE, DIAZEPAM, DIPHENYLHYDANTOIN, FLUNITRAZEPAM AND HALOPERIDOL ON THE VOLTAGE-DEPENDENT SODIUM CURRENT OF ISOLATED MAMMALIAN BRAIN NEURONS Peer-reviewed

    M WAKAMORI, M KANEDA, Y OYAMA, N AKAIKE

    BRAIN RESEARCH　494　(2)　374-378　1989/08

    ISSN： 0006-8993

  69. GABA-INDUCED CHLORIDE CURRENT IN RAT ISOLATED PURKINJE-CELLS Peer-reviewed

    M KANEDA, M WAKAMORI, N AKAIKE

    AMERICAN JOURNAL OF PHYSIOLOGY　256　(6)　C1153-C1159　1989/06

    DOI： 10.1152/ajpcell.1989.256.6.C1153 　

    ISSN： 0002-9513

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    塚本匡顕, 千葉雪絵, 若森実, 日高將文, 山田智士, 角替俊輔, 長由扶子, 榊原良, 今津拓也, 所聖太, 佐竹佳樹, 安立昌篤, 西川俊夫, 山下まり, 此木敬一

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  2. The inhibitory mechanism of eugenol on TRPV1 channel

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    JOURNAL OF PHARMACOLOGICAL SCIENCES　124　175P-175P　2014

    ISSN： 1347-8613

    eISSN： 1347-8648

  3. Cav2.1カルボキシル末端細胞質内ドメインの病態生理学的意義の検討

    相川 知徳, 宮崎 太輔, 三國 貴康, 重本 隆一, 若森 実, 狩野 方伸, 渡邊 雅彦, 水澤 英洋, 渡瀬 啓

    臨床神経学　53　(12)　1495-1495　2013/12

    Publisher: (一社)日本神経学会

    ISSN： 0009-918X

  4. The inhibitory mechanism of eugenol on TRPV1 channel

    Takashi Yoshida, Kaori Takahashi, Takashi Kikuchi, Minoru Wakamori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　121　171P-171P　2013

    ISSN： 1347-8613

  5. 電位依存性チャネル Invited

    若森実, 三木崇史, 中尾章人, 高田宜則, 森泰生

    脳神経科学イラストレイテッド 改訂第3版　2013

  6. The conflicting effects of eugenol on TRPV1 channel

    Takashi Yoshida, Takashi Kikuchi, Kaori Takahashi, Minoru Wakamori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　118　249P-249P　2012

    ISSN： 1347-8613

  7. TRP channels play a role in the mouse osteoblast cell line MC3T3-E1 under shear stress

    Takashi Yoshida, Minoru Wakamori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　115　220P-220P　2011

    ISSN： 1347-8613

  8. Inactivation of voltage-gated CA^2+ channels and cone-rod dystrophy cord7. [Emerging Frontiers in Brain Research: Crossroads of metabolic regulaltion, stress response and disease. The 11th Meeting of Hirosaki International Forum of Medical Science. Communication Center of Hirosaki University School of Medicine. March 27-28,2009. Hirosaki, Japan.]

    Wakamori Minoru, Uriu Yoshitsugu, Miki Takafumi, Kiyonaka Shigeki, Mori Yasuo

    The Hirosaki medical journal　61　S53-S62　2010

    Publisher: Hirosaki University

    ISSN： 0439-1721

  9. Neuronal Ca2+-sensitive non-selective cation channels and TRPC5

    Minoru Wakamori

    Journal of Oral Biosciences　52　(4)　352-357　2010

    Publisher: Japanese Association for Oral Biology

    DOI： 10.2330/joralbiosci.52.352 　

    ISSN： 1349-0079

  10. Modulation of TRPM5 channel activities by fatty acids

    Minoru Wakamori, Takashi Yoshida, Takashi Kikuchi

    JOURNAL OF PHARMACOLOGICAL SCIENCES　112　38P-38P　2010

    ISSN： 1347-8613

  11. ナトリウムチャネル遺伝子Scn1a変異ラットの開発解析研究

    芹川忠夫, 大守伊織, 大内田守, 大野行弘, 鶴見東志子, 三木崇史, 若森実, 石原靜, 吉田卓史, 滝沢明子, 加藤めぐみ, 平林真澄, 笹征史, 森泰生, 真下知士

    てんかん治療研究振興財団研究年報　21　29-36　2010

  12. Expression patterns of mechanosensitive TRP genes in MC3T3-E1 cells

    Takashi Yoshida, Yuki Miyajima, Minoru Wakamori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　109　176P-176P　2009

    ISSN： 1347-8613

  13. FACILITATION OF TRPC5 CHANNEL BY CALCIUM

    Minoru Wakamori, Takashi Yoshida, Shinichiro Yamamoto, Yasuo Mori

    JOURNAL OF PHYSIOLOGICAL SCIENCES　59　396-396　2009

    ISSN： 1880-6546

  14. TRP CHANNELS PLAY A ROLE IN MECHANICAL RESPONSES IN STRETCHED OSTEOBLASTS

    Takashi Yoshida, Yuki Miyajima, Minoru Wakamori

    JOURNAL OF PHYSIOLOGICAL SCIENCES　59　399-399　2009

    ISSN： 1880-6546

  15. Hyperthermia-induced seizure-susceptible rats: a novel model of febrile seizures

    Tomoji Mashimo, Iori Ohmori, Mamoru Ouchida, Yukihiro Ohno, Toshiko Tsurumi, Takafumi Miki, Minoru Wakamori, Yasuo Mori, Tadao Serikawa

    NEUROSCIENCE RESEARCH　65　S47-S47　2009

    DOI： 10.1016/j.neures.2009.09.084 　

    ISSN： 0168-0102

  16. A pyrazole compound selectively inhibits receptor activated TRPC3 channel

    Kenta Kato, Shigeki Kiyonaka, Motohiro Nishida, Masakazu Ishii, Emiko Mori, Takuro Numaga, Takashi Yoshida, Takafumi Miki, Tsutomu Kobayashi, Takashi Morii, Itaru Harnachi, Minoru Wakamori, Yasuo Mori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　106　210P-210P　2008

    ISSN： 1347-8613

  17. Functional impact of RIM family on gating of voltage-dependent Ca2+ channels

    Yoshitsugu Uriu, Minoru Wakamori, Shigeki Kiyonaka, Satoshi Akiyama, Takafumi Miki, Emiko Mori, Yasuo Mori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　106　243P-243P　2008

    ISSN： 1347-8613

  18. Functional analysis of spinocerebellar ataxia type 6 knock-in mice

    T. Tanabe, H. Saegusa, M. Wakamori, Y. Matsuda, J. Wang, Y. Mori, S. Zong

    JOURNAL OF NEUROCHEMISTRY　102　227-227　2007/08

    ISSN： 0022-3042

  19. Functional impact of an active zone scaffolding protein on gating of voltage-dependent calcium channels

    Yoshitsugu Uriu, Minoru Wakamori, Takafumi Miki, Shigeki Kiyonaka, Yasuo Mori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　103　128P-128P　2007

    ISSN： 1347-8613

  20. Active zone scaffolding protein RIM1 confers sustained activity and neurotransmitter vesicle anchoring to presynaptic Ca2+ channels

    Minoru Wakamori, Shigeki Kiyonaka, Takafumi Miki, Yoshitsugu Uriu, Yasuo Mori

    YAKUGAKU ZASSHI-JOURNAL OF THE PHARMACEUTICAL SOCIETY OF JAPAN　127　103-104　2007

    ISSN： 0031-6903

  21. An active zone scaffolding protein functionally associates with presynaptic calcium channels

    Shigeki Kiyonaka, Takafumi Miki, Mio Nonaka, Yoshitsugu Uriu, Minoru Wakamori, Emiko Mori, Yuji Hara, Michel De Waard, Makoto Itakura, Masami Takahashi, Haruhiko Bito, Kevin Campbell, Yasuo Mori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　103　128P-128P　2007

    ISSN： 1347-8613

  22. Multiple phases of modulations of P/Q-type(Ca(v)2.1)Ca2+ channel activity by metabotropic glutamate receptor subtype 1a (mGluR1a)

    Koji Yamazaki, Satoshi Akiyama, Takuro Numaga, Shigetada Nakanishi, Yasuo Mori, Minoru Wakamori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　103　174P-174P　2007

    ISSN： 1347-8613

  23. Functional impact of RIM family sharing C2B domain on gating of voltage-dependent Ca2+ channels

    Yoshitsugu Uriu, Minoru Wakamori, Shigeki Kiyonaka, Takafumi Miki, Emiko Mori, Yasuo Mori

    NEUROSCIENCE RESEARCH　58　S188-S188　2007

    ISSN： 0168-0102

  24. Active zone protein RIM1 functionally associates with presynaptic VDCCs

    Shigeki Kiyonaka, Takafumi Miki, Mio Nonaka, Yoshitsugu Uriu, Minoru Wakamori, Emiko Mori, Yuji Hara, Michel De Waard, Makoto Itakura, Masami Takahashi, Haruhiko Bito, Campbell Kevin, Yasuo Mori

    NEUROSCIENCE RESEARCH　58　S188-S188　2007

    ISSN： 0168-0102

  25. A novel pyrazole derivative selectively inhibits TRPC3 channel.

    Kenta Kato, Shigeki Kiyonaka, Motohiro Nishida, Masakazu Ishi, Emiko Mori, Takuro Numaga, Takashi Yoshida, Takafumi Miki, Tsutomu Kobayashi, Takashi Morii, Itaru Hamachi, Minoru Wakamori, Yasuo Mori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　103　159P-159P　2007

    ISSN： 1347-8613

  26. Effect of RIM 1 on inactivation of neuronal voltage-dependent calcium channels

    Minoru Wakamori, Yoshitsugu Uriu, Takafumi Miki, Shigeki Kiyonaka, Yasuo Mori

    NEUROSCIENCE RESEARCH　58　S189-S189　2007

    ISSN： 0168-0102

  27. The RIM1 mutation associated with an autosomal dominant cone-rod dystrophy, CORD7, alters effects of RIM1 on VDCC currents

    Takafumi Miki, Shigeki Kiyonaka, Yashitugu Uriu, Minoru Wakamori, Emiko Mori, Makoto Itakura, Masami Takahashi, Campbell Kevin, Yasuo Mori

    NEUROSCIENCE RESEARCH　58　S188-S188　2007

    ISSN： 0168-0102

  28. Discovery of novel TRPC channel blockers

    S Kiyonaka, M Nishida, K Kato, M Wakamori, E Mori, M Ishii, T Kobayashi, Y Mori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　100　181P-181P　2006

    ISSN： 1347-8613

  29. Three kinds of modulations of P/Q-type (Ca(v)2.1) Ca2+ channel activity by metabotropic glutamate receptor subtype 1a (mGluR1a)

    K Yamazaki, M Wakamori, N Shigetada, Y Mori

    JOURNAL OF PHARMACOLOGICAL SCIENCES　100　243P-243P　2006

    ISSN： 1347-8613

  30. Inhibitory effects of cilnidipine on peripheral and brain N-type Ca2+ channels expressed in BHK cells

    K Kato, M Wakamori, Y Mori, K Imoto, K Kitamura

    NEUROPHARMACOLOGY　42　(8)　1099-1108　2002/06

    DOI： 10.1016/S0028-3908(02)00053-9 　

    ISSN： 0028-3908

  31. Activation of ATP receptor increases the cytosolic Ca2+ concentration in ventral tegmental area neurons of rat brain

    Masaru Sorimachi, Kazuhiko Yamagami, Minoru Wakomori

    Brain Research　935　(1-2)　129-133　2002/05/10

    DOI： 10.1016/S0006-8993(02)02473-3 　

    ISSN： 0006-8993

  32. Limited intercellular spread of spontaneous Ca2+ signals via gap junctions between mouse chromaffin cells in situ

    Kazuhiko Yamagami, Takashi Moritoyo, Minoru Wakamori, Masaru Sorimachi

    Neuroscience Letters　323　(2)　97-100　2002/04/26

    DOI： 10.1016/S0304-3940(01)02578-2 　

    ISSN： 0304-3940

  33. Transient receptor potential 1 regulates capacitative Ca2+ entry and Ca2+ release from endoplasmic reticulum in B lymphocytes

    Y Mori, M Wakamori, T Miyakawa, M Hermosura, Y Hara, M Nishida, K Hirose, A Mizushima, M Kurosaki, E Mori, K Gotoh, T Okada, A Fleig, R Penner, M Iino, T Kurosaki

    JOURNAL OF EXPERIMENTAL MEDICINE　195　(6)　673-681　2002/03

    DOI： 10.1084/jem.20011758 　

    ISSN： 0022-1007

  34. LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death

    Y Hara, M Wakamori, M Ishii, E Maeno, M Nishida, T Yoshida, H Yamada, S Shimizu, E Mori, J Kudoh, N Shimizu, H Kurose, Y Okada, K Imoto, Y Mori

    MOLECULAR CELL　9　(1)　163-173　2002/01

    DOI： 10.1016/S1097-2765(01)00438-5 　

    ISSN： 1097-2765

  35. Differential nociceptive responses in mice lacking the alpha(IB) subunit of N-type Ca2+ channels

    S Hatakeyama, M Wakamori, M Ino, N Miyamoto, E Takahashi, T Yoshinaga, K Sawada, K Imoto, Tanaka, I, T Yoshizawa, Y Nishizawa, Y Mori, T Niidome, S Shoji

    NEUROREPORT　12　(11)　2423-2427　2001/08

    ISSN： 0959-4965

  36. Differential nociceptive responses in mice lacking the alpha(IB) subunit of N-type Ca2+ channels

    S Hatakeyama, M Wakamori, M Ino, N Miyamoto, E Takahashi, T Yoshinaga, K Sawada, K Imoto, Tanaka, I, T Yoshizawa, Y Nishizawa, Y Mori, T Niidome, S Shoji

    NEUROREPORT　12　(11)　2423-2427　2001/08

    ISSN： 0959-4965

  37. Functional disorders of the sympathetic nervous system in mice lacking the alpha(1B) subunit (Ca-v 2.2) of N-type calcium channels

    M Ino, T Yoshinaga, M Wakamori, N Miyamoto, E Takahashi, J Sonoda, T Kagaya, T Oki, T Nagasu, Y Nishizawa, Tanaka, I, K Imoto, S Aizawa, S Koch, A Schwartz, T Niidome, K Sawada, Y Mori

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA　98　(9)　5323-5328　2001/04

    DOI： 10.1073/pnas.081089398 　

    ISSN： 0027-8424

  38. Functional disorders of the sympathetic nervous system in mice lacking the alpha(1B) subunit (Ca-v 2.2) of N-type calcium channels

    M Ino, T Yoshinaga, M Wakamori, N Miyamoto, E Takahashi, J Sonoda, T Kagaya, T Oki, T Nagasu, Y Nishizawa, Tanaka, I, K Imoto, S Aizawa, S Koch, A Schwartz, T Niidome, K Sawada, Y Mori

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA　98　(9)　5323-5328　2001/04

    DOI： 10.1073/pnas.081089398 　

    ISSN： 0027-8424

  39. Extracellular Ca2+-induced activation of TRP5 channels.

    M Wakamori, T Okada, S Shimizu, H Yamada, K Imoto, Y Mori

    BIOPHYSICAL JOURNAL　80　(1)　244A-244A　2001/01

    ISSN： 0006-3495

  40. The lethal expression of the GluR2flip/GluR4flip AMPA receptor in HEK293 cells

    M Iizuka, S Nishimura, M Wakamori, Akiba, I, K Imoto, EL Barsoumian

    EUROPEAN JOURNAL OF NEUROSCIENCE　12　(11)　3900-3908　2000/11

    DOI： 10.1046/j.1460-9568.2000.00270.x 　

    ISSN： 0953-816X

  41. Spontaneous single-channel activity of neuronal TRP5 channel recombinantly expressed in HEK293 cells

    H Yamada, M Wakamori, Y Hara, Y Takahashi, K Konishi, K Imoto, Y Mori

    NEUROSCIENCE LETTERS　285　(2)　111-114　2000/05

    DOI： 10.1016/S0304-3940(00)01033-8 　

    ISSN： 0304-3940

  42. A gating charge defect in the voltage sensor of P/Q-type Ca2+ channels is associated with the ataxic mouse mutation rolling Nagoya(tgrol.(jointly worked)

    Journal of Neuroscience　20　5654-5662　2000

  43. 電位依存性チャネル『脳神経科学イラストレイテッド』(共著)

    羊土社　145-151　2000

  44. A gating charge defect in the voltage sensor of P/Q-type Ca2+ channels is associated with the ataxic mouse mutation rolling Nagoya(tgrol.(jointly worked)

    Journal of Neuroscience　20　5654-5662　2000

  45. Stable expression of human homomeric and heteromeric AMPA receptor subunits in HEK293 cells

    S Nishimura, M Iizuka, M Wakamori, Akiba, I, K Imoto, EL Barsoumian

    RECEPTORS & CHANNELS　7　(2)　139-150　2000

    ISSN： 1060-6823

  46. Auxiliary subunits operate as a molecular switch in determining gating behaviour of the unitary N-type Ca2+ channel current in Xenopus oocytes

    M Wakamori, G Mikala, Y Mori

    JOURNAL OF PHYSIOLOGY-LONDON　517　(3)　659-672　1999/06

    DOI： 10.1111/j.1469-7793.1999.0659s.x 　

    ISSN： 0022-3751

  47. Pharmacology of N-type Ca2+ channels distributed in cardiovascular system (Review)

    H Uneyama, A Takahara, M Wakamori, Y Mori, R Yoshimoto

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE　3　(5)　455-466　1999/05

    ISSN： 1107-3756

    eISSN： 1791-244X

  48. Alteration of p-type channel function by tottering mutations

    M Wakamori, K Yamazaki, T Teramoto, T Mori, K Imoto

    BIOPHYSICAL JOURNAL　76　(1)　A93-A93　1999/01

    ISSN： 0006-3495

  49. Direct alteration of the P/Q type Ca2+ channel property by polyglutamine expansion in spinocerebellar ataxia 6(SCA6).(jointly worked)

    Journal of Neuroscience　19　RC14,1-5　1999

  50. Auxiliary subunits operate as a molecular switch in determing gating behaviour of unitary N-type Ca2+ channel currents.(jointly worked)

    Journal of Physiology　517　659-672　1999

    DOI： 10.1111/j.1469-7793.1999.0659s.x 　

  51. Single tottering mutations responsible for the neuropathic phenotype of the P-type calcium channel

    Minoru Wakamori, Kazuto Yamazaki, Hiroshi Matsunodaira, Tetsuyuki Teramoto, Isao Tanaka, Tetsuhiro Niidome, Kouhei Sawada, Yukio Nishizawa, Naomi Sekiguchi, Emiko Mori, Yasuo Mori, Keiji Imotot

    Journal of Biological Chemistry　273　(52)　34857-34867　1998/12/25

    DOI： 10.1074/jbc.273.52.34857 　

    ISSN： 0021-9258

  52. Differential interactions of the C terminus and the cytoplasmic I-II loop of neuronal Ca2+ channels with G-protein alpha and beta gamma subunits - I. Molecular determination

    T Furukawa, T Nukada, Y Mori, M Wakamori, Y Fujita, H Ishida, K Fukuda, S Kato, M Yoshii

    JOURNAL OF BIOLOGICAL CHEMISTRY　273　(28)　17585-17594　1998/07

    DOI： 10.1074/jbc.273.28.17585 　

    ISSN： 0021-9258

  53. Differential interactions of the C terminus and the cytoplasmic I-II loop of neuronal Ca2+ channels with G-protein alpha and beta gamma subunits - I. Molecular determination

    T Furukawa, T Nukada, Y Mori, M Wakamori, Y Fujita, H Ishida, K Fukuda, S Kato, M Yoshii

    JOURNAL OF BIOLOGICAL CHEMISTRY　273　(28)　17585-17594　1998/07

    DOI： 10.1074/jbc.273.28.17585 　

    ISSN： 0021-9258

  54. Halothane increases the open probability of glycine-activated channel current in rat central neurones

    M Wakamori, Y Ikemoto, M Yamashita

    BRITISH JOURNAL OF ANAESTHESIA　80　(6)　840-842　1998/06

    ISSN： 0007-0912

  55. Molecular cloning and functional characterization of a novel receptor-activated TRP Ca2+ channel from mouse brain

    T Okada, S Shimizu, M Wakamori, A Maeda, T Kurosaki, N Takada, K Imoto, Y Mori

    JOURNAL OF BIOLOGICAL CHEMISTRY　273　(17)　10279-10287　1998/04

    DOI： 10.1074/jbc.273.17.10279 　

    ISSN： 0021-9258

  56. Functional characterization of ion permeation pathway in the N-type Ca2+ channel

    M Wakamori, M Strobeck, T Niidome, T Teramoto, K Imoto, Y Mori

    JOURNAL OF NEUROPHYSIOLOGY　79　(2)　622-634　1998/02

    DOI： 10.1152/jn.1998.79.2.622 　

    ISSN： 0022-3077

  57. TRP subtypes are responsible for capasitive calcium entry in distinct mouse brain neurons.(jointly worked)

    NeuroReport　9　507-515　1998

  58. Functional characterization of ion permeation pathway in the N-type Ca2+ channel.(jointly worked)

    Journal of Neurophysiology　79　622-634　1998

    DOI： 10.1152/jn.1998.79.2.622 　

  59. TRP subtypes are responsible for capasitive calcium entry in distinct mouse brain neurons.(jointly worked)

    NeuroReport　9　507-515　1998

  60. Halothane increases open probability of glycine-activated channel current in rat central neurones.(jointly worked)

    British Journal of Anaesthesia　80　840-842　1998

  61. Molecular pharmacology of voltage-dependent calcium channels

    Y Mori, G Mikala, G Varadi, T Kobayashi, S Koch, M Wakamori, A Schwartz

    JAPANESE JOURNAL OF PHARMACOLOGY　72　(2)　83-109　1996/10

    DOI： 10.1254/jjp.72.83 　

    ISSN： 0021-5198

  62. Distinct sets of G-proteins are responsible for inhibition of Ca2+ channel types.

    M Strobeck, M Wakamori, T Niidome, T Nukada, A Schwartz, Y Mori

    BIOPHYSICAL JOURNAL　70　(2)　SUPM9-SUPM9　1996/02

    ISSN： 0006-3495

    eISSN： 1542-0086

  63. Enantiomeric separation of the sites for DHP agonist and antagonist action on the voltage-dependent calcium channel alpha(1) subunit.

    M He, M Wakamori, A Schwartz

    BIOPHYSICAL JOURNAL　70　(2)　MP181-MP181　1996/02

    ISSN： 0006-3495

    eISSN： 1542-0086

  64. STABLE EXPRESSION AND COUPLING OF CARDIAC L-TYPE CA2+ CHANNELS WITH BETA(1)-ADRENOCEPTORS

    A YATANI, M WAKAMORI, T NIIDOME, S YAMAMOTO, TANAKA, I, Y MORI, K KATAYAMA, S GREEN

    CIRCULATION RESEARCH　76　(3)　335-342　1995/03

    ISSN： 0009-7330

  65. STABLE EXPRESSION AND COUPLING OF CARDIAC L-TYPE CA2+ CHANNELS WITH BETA(1)-ADRENOCEPTORS

    A YATANI, M WAKAMORI, T NIIDOME, S YAMAMOTO, TANAKA, I, Y MORI, K KATAYAMA, S GREEN

    CIRCULATION RESEARCH　76　(3)　335-342　1995/03

    ISSN： 0009-7330

  66. ALTERATION OF CHANNEL CHARACTERISTICS BY EXCHANGE OF PORE-FORMING REGIONS BETWEEN 2 STRUCTURALLY RELATED CA2+ CHANNELS

    A YATANI, A BAHINSKI, M WAKAMORI, SQ TANG, Y MORI, T KOBAYASHI, A SCHWARTZ

    MOLECULAR AND CELLULAR BIOCHEMISTRY　140　(2)　93-102　1994/11

    DOI： 10.1007/BF00926748 　

    ISSN： 0300-8177

  67. STABLE EXPRESSION AND BETA-ADRENERGIC REGULATION OF A CARDIAC L-TYPE CA2+ CHANNEL

    M WAKAMORI, S GREEN, S LIGGETT, A YATANI

    BIOPHYSICAL JOURNAL　66　(2)　A229-A229　1994/02

    ISSN： 0006-3495

  68. Distinctive functional properties of the neuronal BII(class E)calcium channel.(jointly worked)

    Receptors and Channels　2　303-314　1994

  69. Alteration of channel characteristics by exchange of pore-forming regions between two structurally related Ca2+ channels.(jointly worked)

    Molecular and Cellular Biochemistry　140　(2)　93-102　1994

    DOI： 10.1007/BF00926748 　

    ISSN： 0300-8177

  70. DISTINCTIVE FUNCTIONAL-PROPERTIES OF THE NEURONAL BII (CLASS-E) CALCIUM-CHANNEL

    M WAKAMORI, T NIIDOME, D FURUTAMA, T FURUICHI, K MIKOSHIBA, Y FUJITA, TANAKA, I, K KATAYAMA, A YATANI, A SCHWARTZ, Y MORI

    RECEPTORS & CHANNELS　2　(4)　303-314　1994

    ISSN： 1060-6823

  71. SINGLE-CHANNEL ANALYSIS OF A CLONED HUMAN HEART L-TYPE CA2+ CHANNEL ALPHA(1)-SUBUNIT AND THE EFFECTS OF A CARDIAC BETA-SUBUNIT

    M WAKAMORI, G MIKALA, A SCHWARTZ, A YATANI

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　196　(3)　1170-1176　1993/11

    DOI： 10.1006/bbrc.1993.2374 　

    ISSN： 0006-291X

  72. SINGLE-CHANNEL ANALYSIS OF A CLONED HUMAN HEART L-TYPE CA2+ CHANNEL ALPHA(1)-SUBUNIT AND THE EFFECTS OF A CARDIAC BETA-SUBUNIT

    M WAKAMORI, G MIKALA, A SCHWARTZ, A YATANI

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　196　(3)　1170-1176　1993/11

    DOI： 10.1006/bbrc.1993.2374 　

    ISSN： 0006-291X

  73. SINGLE-CHANNEL ANALYSIS OF A CLONED HUMAN HEART L-TYPE CA2+ CHANNEL ALPHA(1)-SUBUNIT AND THE EFFECTS OF A CARDIAC BETA-SUBUNIT

    G MIKALA, M WAKAMORI, A SCHWARTZ, A YATANI

    CIRCULATION　88　(4)　277-277　1993/10

    ISSN： 0009-7322

  74. ALTERATION OF CHANNEL CHARACTERISTICS BY EXCHANGE BETWEEN 2 STRUCTURALLY RELATED CA2+ CHANNELS

    A YATANI, A BAHINSKI, S TANG, M WAKAMORI, Y MORI, A SCHWARTZ

    CIRCULATION　88　(4)　277-277　1993/10

    ISSN： 0009-7322

  75. BLOCK OF TRANSIENT OUTWARD-TYPE CLONED CARDIAC K+ CHANNEL CURRENTS BY QUINIDINE

    A YATANI, M WAKAMORI, G MIKALA, A BAHINSKI

    CIRCULATION RESEARCH　73　(2)　351-359　1993/08

    ISSN： 0009-7330

  76. CLONING, CHROMOSOMAL LOCALIZATION, AND FUNCTIONAL EXPRESSION OF THE ALPHA-1-SUBUNIT OF THE L-TYPE VOLTAGE-DEPENDENT CALCIUM-CHANNEL FROM NORMAL HUMAN HEART

    D SCHULTZ, G MIKALA, A YATANI, DB ENGLE, DE ILES, B SEGERS, RJ SINKE, DO WEGHUIS, U KLOCKNER, M WAKAMORI, JJ WANG, D MELVIN, G VARADI, A SCHWARTZ

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA　90　(13)　6228-6232　1993/07

    DOI： 10.1073/pnas.90.13.6228 　

    ISSN： 0027-8424

  77. HYPERPOLARIZING MUSCARINIC RESPONSES OF FRESHLY DISSOCIATED RAT HIPPOCAMPAL CA1 NEURONS

    M WAKAMORI, H HIDAKA, N AKAIKE

    JOURNAL OF PHYSIOLOGY-LONDON　463　585-604　1993/04

    ISSN： 0022-3751

  78. CHARACTERIZATION OF SINGLE-CHANNEL PROPERTIES OF A CLONED CARDIAC TRANSIENT OUTWARD TYPE-K+ CHANNEL (RHK1)

    M WAKAMORI, A YATANI

    BIOPHYSICAL JOURNAL　64　(2)　A393-A393　1993/02

    ISSN： 0006-3495

  79. A NEW TYPE OF CA-2+ CHANNEL BLOCKER, NC-1100, INHIBITS THE LOW-THRESHOLD AND HIGH-THRESHOLD CA-2+ CURRENTS IN THE RAT CNS NEURONS

    N MIYAKE, M WAKAMORI, N AKAIKE

    BRAIN RESEARCH　598　(1-2)　215-220　1992/12

    ISSN： 0006-8993

  80. CLONING AND EXPRESSION OF NORMAL HUMAN HEART L-TYPE VOLTAGE-DEPENDENT CA2+ CHANNEL (L-VDCC) - ALPHA-1-BETA-INTERACTION

    G MIKALA, A YATANI, D SCHULTZ, M WAKAMORI, G VARADI, A SCHWARTZ

    CIRCULATION　86　(4)　76-76　1992/10

    ISSN： 0009-7322

  81. MOLECULAR MECHANISMS OF QUINIDINE INHIBITION OF A CLONED HEART TRANSIENT OUTWARD K+ CHANNEL

    A YATANI, M WAKAMORI, A SCHWARTZ

    CIRCULATION　86　(4)　616-616　1992/10

    ISSN： 0009-7322

  82. VOLTAGE-DEPENDENT CURRENTS IN ISOLATED SINGLE MERKEL CELLS OF RATS

    Y YAMASHITA, N AKAIKE, M WAKAMORI, IKEDA, I, H OGAWA

    JOURNAL OF PHYSIOLOGY-LONDON　450　143-162　1992/05

    ISSN： 0022-3751

  83. EFFECTS OF 2 VOLATILE ANESTHETICS AND A VOLATILE CONVULSANT ON THE EXCITATORY AND INHIBITORY AMINO-ACID RESPONSES IN DISSOCIATED CNS NEURONS OF THE RAT

    M WAKAMORI, Y IKEMOTO, N AKAIKE

    JOURNAL OF NEUROPHYSIOLOGY　66　(6)　2014-2021　1991/12

    ISSN： 0022-3077

  84. GAMMA-AMINOBUTYRIC ACID-INDUCED RESPONSE IN ACUTELY ISOLATED NUCLEUS-SOLITARII NEURONS OF THE RAT

    T NAKAGAWA, M WAKAMORI, T SHIRASAKI, T NAKAYE, N AKAIKE

    AMERICAN JOURNAL OF PHYSIOLOGY　260　(4)　C745-C749　1991/04

    ISSN： 0002-9513

  85. DUAL EFFECT OF GLYCINE ON ISOLATED RAT SUPRACHIASMATIC NEURONS

    C ITO, M WAKAMORI, N AKAIKE

    AMERICAN JOURNAL OF PHYSIOLOGY　260　(2)　C213-C218　1991/02

    ISSN： 0002-9513

  86. γ-Aminobutyric acid-induced response in acutely isolated nucleus tractus solitarii neurons of the rat.(jointly worked)

    American Journal of Physiology　260　C745-C749　1991

  87. Dual effect of glycine on isolated rat suprachiasmatic neurons.(jointly worked)

    American Journal of Physiology　260　C213-C218　1991

  88. EXCITATORY AMINO-ACID RESPONSE IN ISOLATED NUCLEUS TRACTUS SOLITARII NEURONS OF THE RAT

    T NAKAGAWA, T SHIRASAKI, M WAKAMORI, A FUKUDA, N AKAIKE

    NEUROSCIENCE RESEARCH　8　(2)　114-123　1990/06

    DOI： 10.1016/0168-0102(90)90063-K 　

    ISSN： 0168-0102

  89. LOW-THRESHOLD CALCIUM CURRENT IN ISOLATED PURKINJE-CELL BODIES OF RAT CEREBELLUM

    M KANEDA, M WAKAMORI, C ITO, N AKAIKE

    JOURNAL OF NEUROPHYSIOLOGY　63　(5)　1046-1051　1990/05

    ISSN： 0022-3077

  90. GLYCINE-INSENSITIVE DESENSITIZATION OF N-METHYL-D-ASPARTATE RECEPTORS IN ACUTELY ISOLATED MAMMALIAN CENTRAL NEURONS

    T SHIRASAKI, T NAKAGAWA, M WAKAMORI, N TATEISHI, A FUKUDA, K MURASE, N AKAIKE

    NEUROSCIENCE LETTERS　108　(1-2)　93-98　1990/01

    ISSN： 0304-3940

  91. Glycine-insensitive desensitization of N-methyl-D-aspartate receptors in acutely isolated mammalian central neurons.(jointly worked)

    Neuroscience Letters　108　93-98　1990

  92. HIPPOCAMPAL CA1 PYRAMIDAL CELLS OF RATS HAVE 4 VOLTAGE-DEPENDENT CALCIUM CONDUCTANCES

    K TAKAHASHI, M WAKAMORI, N AKAIKE

    NEUROSCIENCE LETTERS　104　(1-2)　229-234　1989/09

    ISSN： 0304-3940

  93. EFFECTS OF CHLORDIAZEPOXIDE, CHLORPROMAZINE, DIAZEPAM, DIPHENYLHYDANTOIN, FLUNITRAZEPAM AND HALOPERIDOL ON THE VOLTAGE-DEPENDENT SODIUM CURRENT OF ISOLATED MAMMALIAN BRAIN NEURONS

    M WAKAMORI, M KANEDA, Y OYAMA, N AKAIKE

    BRAIN RESEARCH　494　(2)　374-378　1989/08

    ISSN： 0006-8993

  94. GABA-INDUCED CHLORIDE CURRENT IN RAT ISOLATED PURKINJE-CELLS

    M KANEDA, M WAKAMORI, N AKAIKE

    AMERICAN JOURNAL OF PHYSIOLOGY　256　(6)　C1153-C1159　1989/06

    ISSN： 0002-9513

  95. Kinetic analysis of the GABA-induced chloride current in cerebellar Purkinje cells

    KANEDA MAKOTO, Wakamori Minoru, Akaike Norio

    Acta Physiologica Scandinavica　136　71　1989

  96. GABA-induced chloride current in rat isolated Purkinje cells.(jointly worked)

    American Journal of Physiology　256　C1153-C1159　1989

  97. Two cases of erectile hemangioma in the masseter muscle.

    WAKAMORI Minoru, KAWANO Yoshiharu, ISHII Tomoyuki, KURIYAMA Kanji, KATSUYAMA Hideaki, ENOMOTO Takashi, SHINOHARA Masanori, TAKENOSHITA Yasuharu, OKA Masuichiro

    Journal of Oral Surgery Society of Japan　35　(1)　217-220　1988

    Publisher: Japanese Society of Oral and Maxillofacial Surgeons

    DOI： 10.5794/jjoms.35.217 　

    ISSN： 0021-5163

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    Intramuscular hemangiomas of the head and neck region occur in approximately 10% of all intramuscular hemangiomas. Erectile hemangiomas in the masseter are characterized by exhibiting the swelling not at the rest of the mandible, but at the biting.<BR>We have observed two erectile hemangiomas. The first case was a 27 year old female and the second was a 35 year old female. We extirpated the tumors in the first case from the extraoral and in the second from the intraoral. In the second case the size of the tumor reduced within 5 years of follow-up, and we experienced difficulty of recognition of the hemangioma in the operation. In general, venous hemangiomas don't reduce in size but in the second case we made a diagnosis of a venous hemangioma.

  98. Experiences of the treatments for the mandibular angle fracture.

    KATSUYAMA Hideaki, TAKENOSITA Yasuharu, WAKAMORI Minoru, YOSHIDA Atsuya, KAJIOKA Shunichi, ABE Kihachiro, TANAKA Youichi, KURIYAMA Kanji, KAWANO Yoshiharu, OKA Masuichiro

    Journal of Oral Surgery Society of Japan　34　(7)　1387-1393　1988

    Publisher: Japanese Society of Oral and Maxillofacial Surgeons

    DOI： 10.5794/jjoms.34.1387 　

    ISSN： 0021-5163

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    Mandibular fracture treatment occupies a large part of oral surgery in hospital practice, yet much confusion exists in certain basic principles of treatment.<BR>Mandibular angle is known to be one of the most fractured areas in oral surgery because of its configuration and the common fracturing vectors. One big problem exists in dealing with teeth on the fracture line. Some authors consider any fracture through the alveolar socket or the crypt of an impacted tooth as a "complicated" fracture and say that the involved teeth even though uninjured should be extracted promptly because they may be the cause of complications such as nonuion, osteomyelitis, cellulitis or abscess formation. On the other hand, it is suggested that with the use of antibiotics and the application of stable fixation appliances, most clinically intact teeth in the line of mandibular fracture can be retained. From 1978 to MAY 1987, we treated 57 cases of mandibular angle fractures and analyzed the data with special reference to third molar teeth on the fracture line, types of fracture line, and way of approach and treatment.<BR>The majority of cases consisted of males (51/57, 89.5%), and were between 10 and 20 years old (68%).<BR>Some researchers mentionend that treatment for third molar teeth on the fracture line, but it is rare. So we considered this matter in more details. We, furthermore, examined fracture displacements of fragments, and so on.

  99. Bidirectional alteration in cerebellar synaptic transmission of tottering and rolling Ca2+ channel mutant mice.(jointly worked)

    Journal of Neuroscience　22　4388-4398

  100. Activation of ATP receptor increases the cytosolic Ca2+ concentration in ventral tegmental area neurons of rat brain(jointly worked)

    Brain Research　935　129-133

    DOI： 10.1016/S0006-8993(02)02473-3 　

  101. Bidirectional alteration in cerebellar synaptic transmission of tottering and rolling Ca2+ channel mutant mice.(jointly worked)

    Journal of Neuroscience　22　4388-4398

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Research Projects 27

  1. Molecular mechanisms of Epiprofin in dental epithelial cells.

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tohoku University

    2024/04/01 - 2027/03/31

  2. 唾液腺発生における神経-器官相互作用の分子機構の解明と機能再生技術への応用

    中村 卓史, 若森 実, 中村 はな, 真藤 裕基, 千葉 雄太

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 国際共同研究加速基金(国際共同研究強化(B))

    Institution: 東北大学

    2021/10/07 - 2025/03/31

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    歯、毛包、腺組織、腎臓、肺、消化管組織に存在する上皮組織は、共通性のある上皮間葉相互作用により発生し、転写因子エピプロフィン（Epfn）は上皮細胞の増殖、枝分かれ、運命決定、組織幹細胞維持、細胞死を制御し上皮組織の発生形態形成、また皮膚、毛包などでは組織恒常性維持のため幹細胞維持とTransient-amplifying (TA)細胞の増殖と運命決定に重要である。完成した器官が、支配神経制御下で生体機能を発揮するためには、器官形成時に神経終末が効果器となる細胞（唾液腺では主に筋上皮細胞）に隣接して分化誘導され組織内に配置される必要がある。すなわち自律神経制御を受ける唾液腺は、器官完成後分泌を促進させる指令を出す副交感神経とその指令を受け唾液を分泌させるために腺房・導管を収縮させる筋上皮細胞が近接されて器官設計されることが必要である。これらの器官形成には、歯、毛包、腺組織、腎臓、肺、消化管組織形成期に展開される共通性のある上皮間葉相互作用が重要である。転写因子エピプロフィン（Epfn）は上皮細胞の増殖、枝分かれ、運命決定、組織幹細胞維持、細胞死を制御しているが、神経―上皮組織間の相互作用にも関与している事が、強く示唆される結果を得た。本研究の目的は、唾液腺器官培養系を用いて神経伝達物質とEpfnがどのように共役し、唾液腺上皮細胞の増殖と運命決定と組織内の細胞配置を制御しているのかを解明することであり、海外共同研究では、放射線照射モデルを利用し、障害唾液腺の再生を発生過程での神経伝達物質とEpfnの作用を応用することによる効果的で機能的な再生器官誘導法樹立への道筋をたてることである。

  3. エピプロフィンによる上皮間葉転換制御機構を応用したがん治療と器官原器複製術の開発

    中村 卓史, 中村 はな, 若森 実

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(C)

    Institution: 東北大学

    2021/04/01 - 2024/03/31

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    本研究は、器官形成期に一部の細胞集団が一塊となり細胞遊走能を獲得し間葉組織へと陥入し器官原器を形成する機構の解明のみならず、1つの歯堤から複数の歯胚や後続永久歯胚の形成機構、毛包器官のself-renewing機構の解明の一助になる。また、がん細胞がEMT状態へ移行し、細胞遊走能を活性化しそして転移する新たなメカニズムの解明にもつながるのではないかと考えている。また、本研究は転移しないがん細胞への形質転換治療という新たな治療法や器官原器数を増やす器官再生技術の開発を目指し、Epfnの発現制御に関わる小分子化合物をリード化合物として誘導体を合成し、新規物質の創製などへの研究の発展性もある。 上皮細胞が移動能を有する間葉細胞に転換する上皮間葉転換(Epithelial to mesenchymal transition; EMT)は、胚の初期発生や器官形成に重要である。この現象は発生時のみならず、創傷治癒、腫瘍細胞の転移などでも起こり、EMTに関連する蛋白は、がんのバイオマーカーにも使われている。転写因子エピプロフィン(Epfn)発現が欠失した上皮および歯原性上皮細胞は、細胞移動能が亢進し間葉への上皮陥入が継続する。つまりEpfnはEMTを負に制御していることが示唆される。以上のことから本研究では細胞遊走・移動におけるEpfnの役割解明を目的とする。さらにEpfn発現を人為的に操作し上皮細胞の遊走を制御することにより、新たながん治療法や器官原器複製による再生技術の開発基盤となる知見獲得を目指す 。

  4. 臨床ゲノム研究に基づく非興奮性細胞における電位依存性カルシウムチャネル機能の解明

    若森 実, 中村 卓史

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(C)

    Institution: 東北大学

    2020/04/01 - 2023/03/31

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    「非興奮性細胞の膜電位は変動するか？」を明らかにするために、非興奮性細胞である骨芽細胞様細胞MC3T3-E1細胞にパッチクランプ法を適用し、静止膜電位を計測すると平均は-7.7 ± 0.7 mV (n = 25)であった。1 mM Zn2+を投与すると、２種類の過分極応答が記録できた。-6.1 ± 0.6 mVの膜電位が-14.2 ± 1.1 mV (n = 9)まで過分極したグループと、-8.5 ± 1.1 mVの膜電位が-64.6± 1.3 mV (n = 16)まで過分極したグループに分類できた。前者では膜抵抗が上がっていたため、非選択的陽イオンチャネルが遮断されて過分極したことが判明した。一方、後者では膜抵抗が下がっていたため、K+チャネルが開口して過分極したことが判明した。K+チャネル開口の細胞内機構を薬理学的・分子生物学的に検討した。K+チャネルの開口には細胞内Ca2+が必要であり、RT-PCR法によりSK、IK、BKチャネルが発現していた。ピペット内液にZn2+キレーターを添加するとBKチャネルは活性化されなくなったが、IKチャネルは影響を受けなかった。これはBKチャネルが細胞内のZn2+によって活性化させることを意味する。以上の結果より、生体内に豊富に存在するZn2+がK+チャネルを活性化させることにより非興奮性細胞でも膜電位が大きく変化することが明らかになった。 自閉スペクトラム症に関係する可能性のある新たな変異がCav1.3で発見された。変異部位がポア領域に近いため、ヒト大脳皮質由来のCACNA1DのcDNAをクローニングし、野生型チャネルと変異チャネルをBHK細胞に強制発現させてシングルチャネルコンダクタンスを検討することにした。現在、野生型チャネルの解析が終了し、約23 pSであることが判明した。変異チャネルの解析を進める予定である。

  5. Development and application of optical imaging measurement of brain metabolite clearance characteristics

    Katayama Norihiro

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    2019/04/01 - 2022/03/31

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    This study modified the functional integrative optical imaging (fIOI) method developed by the principal investigators to quantify temporal changes in brain clearance characteristics to improve temporal resolution and signal-to-noise ratio. The improved method was applied to in vivo mice that spontaneously repeat sleep-wake states to quantify the sleep state dependence. The results showed that clearance was more rapid during the sleep phase than during the wake phase. This result is similar to previous reports using real-time micro-iontophoresis. The fIOI experimental system was mathematically modeled, and numerical simulations revealed some of the limitations of the performance of this experimental system.

  6. The development of light-activatable proteins for inducing mechanical stimulation in the cells

    Yoshida Takashi, Wakamori Minoru

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Challenging Exploratory Research

    Institution: Tohoku University

    2015/04/01 - 2018/03/31

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    Vertebrates have the cells which receive the mechanical force from the outer world and translate to the intracellular signaling. However, it is not clear the strength of mechanical stimulation at the local area of the cell and how the signals transduce from cell to cell because these mechanosensory cells are often embedded in the hard tissues like bone. So, we developed the non-contact method to provide mechanical stress in the specified area of the cell by using visible light. We made some light-activatable protein pairs containing LOV domain (light accepting module) and actin-depolymerizing proteins. The expressing vectors of light-activatable proteins were transfected into the MC3T3-E1 cells. The irradiation of blue light to the cells has resulted in a decrease of the actin filament. As this effect is not so remarkably, the improvement of light-activatable proteins is needed.

  7. Pathophysiological analysis of oral diseases caused by dysregulation of cation channels

    Wakamori Minoru

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tohoku University

    2015/04/01 - 2018/03/31

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    We studied the effects of the stimulating ingredients on TRPA1 channel recombinantly expressed in HEK293 cells using the Ca2+ imaging analysis and the patch-clamp technique. Formaldehyde, butylaldehyde, methyl ethyl ketone, and NNK (4-(methylnitrosoamino) -1-(3-pyridyl)-1-butanoe) activated TRPA1 channel, although acetone, crotonaldyhyde, isoprene, and nicotine did not induce Ca2+ transient. Acrylonitrile induced TRPA1 channel current. We examined the responses to the cigarette smoke elements in trigeminal ganglion neurons and human gingival fibroblast 1. TRPA1 channel was expressed in TRG neurons and HGF-1 cells. Similar to the selective TRPA1 agonist allyl isothiocyanate (AITC), the chemical substances contained in the smoke of tobacco increased intracellular Ca2+ concentration, and induced the outwardly rectifying currents. The responses were blocked by the selective TRPA1 antagonist HC-030031. Therefore it is suggested that TRPA1 channel is activated by the ingredients.

  8. Exploring the regulatory mechanism of hypothalamic local circuitry using a mouse line for visualizing CRF neurons by a fluorescent protein

    Itoi Keiichi, WAKAMORI MINORU, SAKIMURA KENJI

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tohoku University

    2014/04/01 - 2017/03/31

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    Hypothalamic local circuitry was examined using the CRF-Venus mouse in which CRF was labeled by modified yellow fluorescent protein. Hypothalamic CRF neurons receive direct glutamatergic and GABAergic inputs, and the glutamatergic EPSC frequency was increased by noradrenaline (NA). Thus, NA acitivates CRF neurons via glutamatergic interneurons in the hypothalamus. The Neo cassette was deleted from the genome of the CRF-Venus mouse, and CRF-VenusDeltaNeo mouse was generated. Venus fluorescent intensity, as well as its specificity for CRF neurons, was much improved. The distribution of CRF neurons in the whole brain of the mouse was disclosed for the first time using the CRF-VenusDeltaNeo.

  9. Drug-delivery-system through ion channels

    WAKAMORI Minoru, YOSHIDA Takashi

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Challenging Exploratory Research

    Institution: Tohoku University

    2013/04/01 - 2015/03/31

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    TRPV1 channel is activated by capsaicin and is permeable to Na+, K+ and Ca2+. Concentration-response relationship for capsaicin was obtained from the HEK293 cells expressing recombinant TRPV1 channel. The threshold concentration and EC50 of capsaicin were 0.03 and 0.22 uM, respectively. FM1-43, a positively charged organic ion, was a permeant when the TRPV1 channel was activated by 1 uM capsaicin, indicating that TRPV1 channel pore size is wide enough to pass the 452 Da FM1-43. When the extracellular Ca2+ was removed, the FM1-43 could not enter the cells through the TRPV1 channel. These results suggest that the TRPV1 channel pore is dilated by capsaicin but extracellular Ca2+ regulates the dilation.

  10. An investigation of the relationship between occlusion, mastication and mental activity using in vivo patch clamp recording method

    TSBUBOI Akito, WAKAMORI Minoru

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tohoku University

    2011 - 2013

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    In this project we try to provide a micropipette for the in vivo patch clamp technique. Unfortunately, few probes were obtained to allow forming the high resistance seal (giga-ohm seal). The other device was also needed to reach the objective neurons of the in vivo specimen. These micropipettes, however, allowed us performing extracellular recording. Neuronal activities responding mechanical stimulation to the oro-facial region were extracellularly recorded from the ventral posteromedial nucleus of the rabbit thalamus. Ninety percent of recorded neurons responded to mechanical stimuli associated with occluding and chewing and also related to the mental activity. These results suggested that sensory information from oro-facial region during occlusion and mastication influences on the level of consciousness.

  11. NETWORK ANALYSIS AMONG HARD TISSUE CELLS USING MULTI-PHOTON MICROSCOPE

    WAKAMORI Minoru, NAKAI Jyunichi

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Challenging Exploratory Research

    Institution: Tohoku University

    2010 - 2012

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    Osteoblasts and bone cells detect mechanical stimuli, and it is thought that their networks share information. The final goal of this project is to establish the method to analyze the network function among the cells by measuring intracellular Ca^<2+> concentration as an index. Ca^<2+> influx was observed in the osteoblast-like cells after extension. Moreover, Ca^<2+> fluorescent proteins worked like Ca^<2+> indicator fura-2.

  12. Functional analysis of oral sensation on the basis of signalplexes

    WAKAMORI Minoru, YOSHIDA Takashi, MORI Yasuo

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (B)

    Institution: Tohoku University

    2009 - 2011

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    Fat is one of the three major nutrients but it is not a sapid substance which activates one of the five basic tastes, sweet, bitter, sour, salt, and umami. However, we have experience that fat changes the taste of dishes largely. Transient receptor potential M5(TRPM5)channel is not a receptor of the five basic tastes but it is gated after stimulation of the gustducin-coupled receptors for sweet, bitter, and umami. We analyzed the electrophysiological and pharmacological properties of TRPM5 channel. TRPM5 channel was not activated by fatty acids, but modulated by fatty acids.

  13. Mechanism of sensory dysfunction of swallowing in elderly people and its applied regenerative therapy

    EBIHARA Satoru, WAKAMORI Minoru

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (B)

    Institution: Tohoku University

    2009 - 2011

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    We found that dysphagia in elderly is mainly due to dysfunction of thermosensing TRP channels. In order to regenerate the function of thermosensing TRP channels, we developed methods to regenerate TRPV1 response using capsiate, non-pungent TRPV1 agonist, and red wine polyphenols, a TRPV1 modulator. By combining methods to regenerate thermosensing TRP channels, we developed a protocol to start eating more efficiently and safely in fasted patients with aspiration pneumonia. Using this protocol, the incidence of pneumonia and the number of febrile days for 1 mont h from the start of oral intake were significantly reduced.

  14. 味覚形成における脂質ミクロドメインの役割

    若森 実

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 特定領域研究

    Institution: 東北大学

    2008 - 2009

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    味蕾に発現するTRPM5チャネルをHEK293細胞に発現させ、アラキドン酸によるTRPM5チャネルの修飾をパッチクランプ法ホールセル法を用いて電気生理学的に検討した。膜電位は-60mVに保持し、3秒毎に80mVから-80mVへの320msのNegative rampをかけることで、電流-電圧関係を記録した。電極内液のフリーCa^<2+>濃度を0.3μMに設定しているため、ホールセル法を確立後に細胞内のCa^<2+>濃度が0.3μMに近づき、徐々にチャネルが活性化され外向き整流性のあるTRPC5チャネル活性が記録できた。細胞外のCa^<2+>を除去すると、チャネル活性が著しく低下した。また、昨年報告した10μMのアラキドン酸で惹起されるチャネル活性も著しく低下した。これは細胞膜に非選択的なリーク電流が存在し、細胞内にCa^<2+>を流入させることによりTRPM5チャネルが活性化された可能性を示唆する。従って、細胞外Ca^<2+>を除去した外液中でアラキドン酸を投与し、脂肪酸のTRPM5チャネルの修飾様式を検討し直した。アラキドン酸は外向き整流性を示し、逆転電位が8mV付近のTRPM5チャネル活性を惹起した。更に、食物中の不飽和脂肪酸でも小さいながらTRPM5チャネルを活性化できることが判明した。しかし、不飽和脂肪酸による修飾は細胞内Ca^<2+>濃度がマイクロモル以下になると認められないことから、不飽和脂肪酸はTRPM5チャネル活性を修飾するにすぎない。

  15. Ca^<2+> channelplexes : assembly in the membrane and physiological significance

    MORI Yasuo, FUJIMOTO Toyoshi, WAKAMORI Minoru, HARA Yuji

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research on Priority Areas

    Institution: Kyoto University

    2005 - 2009

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    Ca^<2+> as a second messenger controls a wide variety of biological responses and contributes to formation of tissues such as bones, thereby playing a central role in regulating "homeostasis" at whole body, tissue, and cell levels. In my research, I have focused on voltage-dependent Ca^<2+> channels (VDCCs) and transient receptor potential (TRP) channels to aim at understanding mechanisms, that underlie formation and assembly at the biomembrane of Ca^<2+> channel protein complexes (Ca^<2+> channelplexes), and their physiological significance. Firstly, I have unveiled several unique activation mechanisms, that regulate cellular signal transduction for TRP Ca^<2+>-permeable caion channels. Secondly, I have demonstrated that channel proteins act not only as Ca^<2+>-permeating apparatus but also as assembly centers for receptors, signal-regulating proteins, and scaffolding proteins. Thirdly, important roles of Ca^<2+> channel protein complexes via formation of feedback regulation pathways in signal transduction have been demonstrated. Finally, I have also shown physiological significance of Ca^<2+> channelplexes at tissue levels. TRPC3 channelplexes in B lymphocyte activation and P/Q type VDCCplexes in presynaptic vesicle fusion are examples of the outcome of this study. Thus, my study clarifies how individual Ca^<2+> channels play roles in unique cellular responses.

  16. 優性及び劣性遺伝形態をとる運動失調症マウスの小脳機能の電気生理学的比較

    若森 実, 森 泰生

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 特定領域研究

    2006 - 2007

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    運動失調症を呈するトタリング(tg)、リーナー(tg^<la>)及びローリングナゴヤ(tg^<rol>)マウスはP型Ca^<2+>チャネルをコードするCav2.1に変異があり、プルキンエ細胞のP型チャネルの活性が低下していることを明らかにしてきた。また、tg、tg^<la>及びtg^<rol>マウスが持つ変異をCav2.1に導入し、BHK細胞に発現させ、パッチクランプ法を用いて急性単離プルキンエ細胞で得られたデータと同様の傾向が見られることを報告してきた。しかし、BHK細胞に発現させたCav2.1チャネルの不活性化は非常に速いのに対し、急性単離プルキンエ細胞のP型チャネル電流の不活性化は遅い。我々はシナプス前膜でシナプス小胞の開口放出に関わるRIM1(Rab3-interacting molecule 1)がCa^<2+>チャネルのβサブユニットと相互作用し、チャネルの不活性化を修飾することを見出した。RIM1(1079-1257)はCa^<2+>チャネルのβサブユニットと弱く結合するが、不活性化を変化させなかった。一方、RIM1(1258-1463)はCa^<2+>チャネルのβサブユニットと弱く結合し不活性化のkineticsを遅くし、定常状態の不活性化曲線を右方移動させた。kinetics及び、不活性化曲線は2段になり、RIM1(1258-1463)が結合したCa^<2+>チャネルと結合していないCa^<2+>チャネルがあるようである。 RIM1(1079-1463)はCa^<2+>チャネルのβサブユニットと強く結合しRIM1全長と同等かそれ以上に不活性化のkineticsを遅くし、定常状態の不活性化曲線を右方移動させた。以上の結果よりアクティブゾーンにあり神経伝達物質放出に係わるRIM1がC末領域で電位依存性Ca^<2+>チャネルのβサブユニットと結合し、不活性化機構の調節を行い、シナプス伝達効率を調節している可能性が示唆された。

  17. 小脳失調症の遺伝子、分子、細胞、小脳回路と多次元コンピュテーショナル神経科学

    若森 実, 森 泰生, 原 雄二

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 特定領域研究

    Institution: 京都大学

    2005 - 2005

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    P型Ca^<2+>チャネルをコードするCav2.1(α_<1A>)に変異が入り、ヒトに於いてEpisodic Ataxia2(EA2)、家族性片麻痺性偏頭痛、遺伝性脊髄小脳変性症(SCA6)等の中枢神経疾患が引き起こされる。我々は運動失調症を呈するtottering(tg)、leaner(tg^<la>)及びrolling Nagoya(tg^<rol>)マウスもα_<1A>サブユニットに変異があり、プルキンエ細胞のP型Ca^<2+>チャネルの活性が低下していることを明らかにした。 本申請研究では、劣性遺伝性運動失調と欠神発作を示すtottering^<4J>(tg^<4J>)と半優性遺伝性運動失調を示すtottering^<5J>(tg^<5J>)の2種類の病態マウスを新たに入手しα_<1A>サブユニットに変位部位を同定し、チャネルの機能解析をパッチクランプ法を用いて行った。まず、α_<1A>サブユニットに変異を導入しα_2/δとβ_4を安定発現させたBHK細胞に強制発現させた。電流量及び電流密度は2種類の変異チャネルと正常チャネルで有意の差が無かった。しかし、tg^<4J>が50%活性化される膜電位(V_<0.5>)はtg^<la>やtg^<rol>同様に正常チャネルと比べて約7mV脱分極側に移動した。一方、tg^<5J>のV_<0.5>は約13mV過分極側に移動した。しかし、逆転電位は変化しなかった。以上のデータより、これら2種類の変異はチャネルのイオン透過性に影響を与えないが、ゲーティングに影響を与えていることが判明した。つまり、tg^<4J>チャネルが開口し難くなっているのに対し、tg^<5J>チャネルが開口し易くなっていることが判明した。今回のマウスを含めて我々が今まで解析してきたα_<1A>サブユニットに変異を持つ運動失調マウスtg、tg^<la>、tg^<rol>、tg^<4J>は全て劣性遺伝でありCa^<2+>チャネル活性が低下している(Loss of Function)のに対し、tg^<5J>マウスは唯一の優性遺伝性病態マウスでありCa^<2+>チャネル活性が亢進している(Gain of Function)ことが運動失調に繋がっている可能性が強く示唆された。

  18. Elecrtophysiological properties of voltage-gated Ca^<2+> channel and other cation channels.

    WAKAMORI Minoru

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    2003 - 2004

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    Ca^<2+> controls diverse cellular processes, including muscle contraction, neurotransmitter release and other forms of secretion, gene expression, and cell proliferation. To evoke these cellular responses, Ca^<2+> influx across the plasma membrane makes a major contribution to augmenting the cytosolic free Ca^<2+> concentration ([Ca^<2+>]_i). In addition to the well-characterized voltage-gated Ca^<2+> channels, ligand-gated channels are the major transmembrane pathways. ATP, the ligand of P2X receptors, is a candidate of neurotransmitter or co-transmitter in the peripheral and central nervous system. Anatomical studies have revealed the wide distribution of P2X receptors in the brain. So far, P2X-mediated synaptic responses have been recorded in a few region of brain. To determine the physiological significance of postsynaptic ATP receptors in the brain, we have investigated the P2X responses in neurons acutely dissociated from rat hypothalamic arcuate nucleus by using the whole-cell mode of the patch-clamp technique. ATP evoked inward currents in a concentration-dependent manner (K_d=42μM) at a holding potential of -70 mV. The current-voltage relationship showed a marked inward rectification starting around -10 mV. Although P2 receptor agonists, 300μM αβ-methylene-ATP and 300μM βγ-methylene-ATP did not induced any current, 100 μM ATPγS and 100μM 2-methylthio-ATP evoked inward currents of which amplitude was 60% of that evoked by 100 μM ATP. PPADS, P2 receptor antagonist, inhibited the ATP-evoked currents in a time- and concentration-dependent manner (K_i=19μM at 2 min). Permeant Ca^<2+> inhibited the ATP-evoked currents in the range of milimolars (K_i=6.9mM), however, Cd^<2+> (1-300 μM), a broad cation channel blocker, facilitated the currents with slow off-rate. Zn^<2+> in the range of 1-20 μM facilitated the current whereas Zn^<2+> at the concentrations over 50 μM inhibited the currents. These observations suggest that functional P2X receptors are expressed in hypothalamic arcuate nucleus.

  19. Functional relationship between Ca^<2+>-dependent cation channel and Ca^<2+>-permeable channel

    WAKAMORI Minoru

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Kagoshima University

    2001 - 2002

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    Ca^<2+> controls diverse cellular processes, which include muscle contraction, neurotransmitter release and other forms of secretion, gene expression, and cell proliferation. To evoke these cellular responses, Ca^<2+> influx across the plasma membrane makes a major contribution to augmenting the cytosolic free Ca^<2+> concentration ([Ca^<2+>]_i). In addition to the well-characterized voltage-gated Ca^<2+> channels and Ca^<2+>-permeable ligand-gated channels, Ca^<2+>-permeable cation channels, activated by downstream of GTP binding protein (G-protein) coupled receptors, have been recognized to be one of the major transmembrane pathways. An important clue to understand the molecular basis of these mammalian Ca^<2+>-permeable cation channels came from the findings of Drosophila visual transduction cascade, since some of the Ca^<2+>-permeable cation channels may be formed by the mammalian homologues of the Drosophila cation channel TRP (the gene product of the transient receptor potential, trp). Currents from HEK cells expressing the TRP3 or the TRP5 were recorded at room temperature using the conventional patch-clamp technique of the whole-cell mode with an Axopatch 200B amplifier. ATP 0.1 mM induced the TRP3 and the TRP5 channel currents at a holding potential of -50 mV in HEK cells expressing the TRP3 and the TRP5, respectively. In the HEK cells expressing the TRP5, extracellular Ca^<2+> at 10 mM induced currents without application of ATP. The current-voltage (I-V) relationships were linear for the TRP3 channel, and outwardly rectified at negative potentials for the TRP5 channel. Ca^<2+> is permeable to TRP5 channel and regulates TRP5 channel.

  20. Dynamic analysis of subcellular ionic signalling in neurons

    IMOTO Keiji, WAKAMORI Minoru, NAKAI Junichi, MORI Yasuo

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (B).

    Institution: Okazaki National Research Institutes

    1999 - 2000

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    We investigated dynamic aspect of local ionic signaling en central neurons, by comparing wild-type and mutant functional molecules or mouse strains. More precisely, we studied molecular biological and electrophysilogical analyses of voltage-gated calcium channels and receptor-activated calcium permeable cation channels. We clarified some steps of the pathogenic mechanism how the calcium channel mutations lead to cerebellar ataxia. Also we showed that receptor-activated calcium permeable channels are expressed in a wide range of tissues including brain, and are critically involved in various aspects of cell regulation. To uncover the pathogenic mechanism of human spinocerebellar ataxia type 6, which has been shown to be associated with CAG nucleotide repeat extension in the P/Q-type calcium channel, we analyzed functional properties of the calcium channel with the extension in a recombinant expression system, to obtain the negative shift of voltage-dependent inactivation. This change is consistent with the idea that reduced calcium influx can be a cause of the cerebellar neuronal disorder. We identified the mutation in the calcium channel α1A gene of the mutant ataxic mouse rolling nagoya. The mutation was located in the voltage sensing region. In fact, the calcium channel was shown to have a reduced voltage sensitivity in addition to reduced current amplitude. This study showed how a single mutation leads to abnormal development and function of the neuronal circuit. The TRP channel is a representative of receptor-activated channels. We conducted molecular analyses of the members of the TRP channel family. The functional properties of TRP channels are characterized using recombinant expression systems. In particular, TRP7, which is constitutively activated without external stimulation, was shown to be functionally similar to the channel previously identified as a calcium permeable non-selective cation channel. The members of TRP channel family may contribute to sustained depolarization of neurons when then receive repetitive stimulations.

  21. Electrophysiological study of mutant P-type Ca^<2+> channels causing diseases

    WAKAMORI Minoru

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Okazaki National Research Institutes

    1999 - 2000

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    An increasing number of disorders have been described in which mutations within voltage-gated ion channels are the underlying molecular defect. Homozygous ataxic mice, tottering (tg) and leaner (tg^<la>) mice, have mutations in the P/Q-type Ca^<2+> channelα_<lA>, subunit gene. Besides these two ataxic mice the third recessive neurological mouse mutant, rolling Nagoya (tg^<rol>), manifests poor motor coordination and stiffness. The rank order of severity of the ataxic symptoms is tg^<la> > tg^<rol> > tg. To explore the relationship between severity of symptoms and channel properties, we have here characterized the electrophysiological properties of Ca^<2+> channels in cerebellar Purkinje cells dissociated from the normal, tg, tg^<la> and tg^<rol> mice. Current density (333 ± 18 pA/pF, n = 67, for normal mice) was significantly reduced in tg^<rol> (247 ± 14, n = 32), tg (184 ± 18, n = 27) and tg^<la> (123 ± 9, n = 25) mice. Peak amplitudes of tail currents, which reflect channel activation, were fitted by a single Boltzmann function, where the voltages for half-maximal activation and slope factors were -28.0 ± 1.1 mV and 4.9 ± 0.5 mV (n = 11) for normal mice, -28.3 ± 1.1 and 4.7 ± 0.3 (n = 13) for tg mice, -20.3 ± 1.7 and 5.8 ± 0.2 (n = 13) for tg^<rol> mice and -19.2 ± 1.3 and 5.4 ± 0.3 (n = 13) for tg^<la> mice, respectively. Activation curves for tg^<rol> and tg^<la> were shifted in the depolarizing direction resulting in reduction of Ca^<2+> channel activity, although it remained normal in tg mice. The results suggest that current reduction and deviation of gating behavior synergically diminish P-type Ca^<2+> channel activity in cerebellar Purkinje cells and may contribute to the neuropathology of the ataxic mice.

  22. Study of electrophysiological properties of cloned N-type Ca^<2+> channel

    WAKAMORI Minoru

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Okazaki National Research Institutes

    1997 - 1998

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    To establish ion conducting properties of the N-type Ca^<2+> channel, we examined a recombinant N-type Ca^<2+> channels expressed in baby hamster kidney cells, using a conventional whole-cell patch-clamp technique.The recombinant N-type Ca^<2+> channel, composed of the alpha_<1B>, alpha_<1*> and beta_<1*> subunits, displayed high-voltage-activated Ba^<2+> currents, and were strongly blocked by the N-type channel blocker omega-conotoxin-GVIA.In the presence of 110mM Ba^<2+>, the unitary current showed a slope conductance of 18.2pS, characteristic of N-type channels. Ca^<2+> and Sr^<2+> resulted in smaller ion fluxes than Ba^<2+>, with the ratio 1.0 : 0.72 : 0.75 of maximum conductance in current-voltage relationships of Ba^<2+>, Ca^<2+> and Sr^<2+> currents, respectively. In mixtures of Ba^<2+> and Ca^<2+>, where the Ca^<2+> concentration was steadily increased in place of Ba^<2+>, with the total concentration of Ba^<2+> and Ca^<2+> held constant at 3mM, the current amplitude went through a clear minimum when 20% of the external Ba^<2+> was replaced by Ca^<2+>.This anomalous mole fraction effect suggests an ion-binding site where two or more permeant ions can sit simultaneously.Using an external solution containing 110mM Na^+ without polyvalent cations, inward Na^+ currents were evoked by test potentials more positive than -5OmV.These currents were activated and inactivated in a kinetic manner similar to that of Ba^<2+> currents.Application of inorganic Ca^<2+> antagonists blocked Ba^<2+> currents through N-type channels in a concentration-dependent manner.The rank order of inhibition was La^<3+> <greater than or equal> Cd^<2+> * Zn^<2+> * Ni^<2+> <greater than or equal> Co^<2+>.When a short strong depolarization was applied before test pulses of moderate depolarizing potentials, relief from channel blockade by La^<3+> and Cd^<2+>, and subsequent channel reblocking was observed.The measured rate (2x10^8M^<-1>s^<-1>) of reblocking approached the diffusion-controlled limit.These results suggest that N-type Ca^<2+> channels share general features of a high affinity ion-binding site with the L-type Ca^<2+> channel, and that this site is easily accessible from the outside of the channel pore. channel calcium patch-clamp omega-conotoxin-GVIA

  23. Production & analysis of Ca^<2+> channel subunit-defecient mice.

    IMOTO Keiji, BEAM Kurt G, SCHWARTZ Arnold, WAKAMORI Minoru, NAKAI Junichi, MORI Yasuo

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for international Scientific Research

    Institution: National Institute for Physiological Sciences

    1997 - 1998

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    We have characterized functional defects of the P/Q-type Ca2^<2+> channels induced by the ataxic mutations tottering (tg) and leaner (tg-la) in the pore-forming alpha_<14> (BI) subunit. Of these two mutations, tg-la which causes more sever ataxia affected biophysical properties of the P/Q-typeCa2^<2+> channel more seriously than the other. The stargazer gene whose mutation cause also epilepsy and ataxia was shown to encode a novel neuronal gamma isoform gamma_2. The interaction sites of the G protein subunits and intracellular Ca2^<2+> release channel (ryanodine receptor)were mapped in the cytoplasmic regions of the Ca2^<2+> channel alpha1 subunits. In addition, we isolated a novel receptor-activated channel TRP5 from mouse brain. TRP5 was activated by receptor stimulation via a mechanism unrelated to store depletion.

  24. 電位依存性カルシウムチャネルの分子神経生理学的研究 Competitive

  25. カルシウム透過型カチオンチャネルの分子神経生理学的研究 Competitive

  26. Molecular and neurophysiological study on voltage-dependent Calcium Channel Competitive

  27. Molecular and neurophysiological Study on Calcium permeable Cation Channels Competitive

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