Toru Kobayashi

Summary

Affiliation: Niigata University
Country: Japan

Publications

  1. ncbi request reprint Modulators of G protein-activated inwardly rectifying K+ channels: potentially therapeutic agents for addictive drug users
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Niigata, Niigata 951 8585, Japan
    Ann N Y Acad Sci 1025:590-4. 2004
  2. ncbi request reprint G protein-activated inwardly rectifying potassium channels as potential therapeutic targets
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, 1 757 Asahimachi, Niigata, Niigata 951 8585, Japan
    Curr Pharm Des 12:4513-23. 2006
  3. pmc Inhibition of g protein-activated inwardly rectifying k channels by phencyclidine
    Toru Kobayashi
    Division of Psychobiology, Tokyo Institute of Psychiatry, 2 1 8 Kamikitazawa, Setagaya Ku, Tokyo 156 8585, Japan
    Curr Neuropharmacol 9:244-6. 2011
  4. pmc Inhibition of G protein-activated inwardly rectifying K+ channels by different classes of antidepressants
    Toru Kobayashi
    Department of Project Programs, Center for Bioresource based Researches, Brain Research Institute, Niigata University, Niigata, Japan
    PLoS ONE 6:e28208. 2011
  5. pmc Inhibition of G-protein-activated inwardly rectifying K+ channels by the selective norepinephrine reuptake inhibitors atomoxetine and reboxetine
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Chuo Ku, Niigata, Japan
    Neuropsychopharmacology 35:1560-9. 2010
  6. pmc Pregnenolone sulfate potentiates the inwardly rectifying K channel Kir2.3
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Niigata, Niigata, Japan
    PLoS ONE 4:e6311. 2009
  7. doi request reprint Inhibitory effects of the antiepileptic drug ethosuximide on G protein-activated inwardly rectifying K+ channels
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, 1 757 Asahimachi, Chuo Ku, Niigata, Niigata 951 8585, Japan
    Neuropharmacology 56:499-506. 2009
  8. ncbi request reprint Inhibition by cocaine of G protein-activated inwardly rectifying K+ channels expressed in Xenopus oocytes
    Toru Kobayashi
    Division of Psychobiology, Tokyo Institute of Psychiatry, 2 1 8 Kamikitazawa, Setagaya Ku, Tokyo 156 8585, Japan
    Toxicol In Vitro 21:656-64. 2007
  9. ncbi request reprint Inhibition of G protein-activated inwardly rectifying K+ channels by the antidepressant paroxetine
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Niigata, Japan
    J Pharmacol Sci 102:278-87. 2006
  10. pmc Functional characterization of an endogenous Xenopus oocyte adenosine receptor
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, 1 757 Asahimachi, Niigata, Niigata 951 8585, Japan
    Br J Pharmacol 135:313-22. 2002

Collaborators

Detail Information

Publications18

  1. ncbi request reprint Modulators of G protein-activated inwardly rectifying K+ channels: potentially therapeutic agents for addictive drug users
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Niigata, Niigata 951 8585, Japan
    Ann N Y Acad Sci 1025:590-4. 2004
    ..Therefore, GIRK channel modulators might be potential agents for the treatment of users of addictive drugs, such as cocaine, opioids, cannabinoids, and ethanol, as well as for the treatment of epilepsy and pain...
  2. ncbi request reprint G protein-activated inwardly rectifying potassium channels as potential therapeutic targets
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, 1 757 Asahimachi, Niigata, Niigata 951 8585, Japan
    Curr Pharm Des 12:4513-23. 2006
    ..We also review the possible roles of GIRK channels in the pathophysiology of various disorders, and discuss the therapeutic potential of GIRK channel modulation...
  3. pmc Inhibition of g protein-activated inwardly rectifying k channels by phencyclidine
    Toru Kobayashi
    Division of Psychobiology, Tokyo Institute of Psychiatry, 2 1 8 Kamikitazawa, Setagaya Ku, Tokyo 156 8585, Japan
    Curr Neuropharmacol 9:244-6. 2011
    ..The results suggest that partial inhibition of GIRK channels by PCP may contribute to some of the toxic effects after overdose...
  4. pmc Inhibition of G protein-activated inwardly rectifying K+ channels by different classes of antidepressants
    Toru Kobayashi
    Department of Project Programs, Center for Bioresource based Researches, Brain Research Institute, Niigata University, Niigata, Japan
    PLoS ONE 6:e28208. 2011
    ..The present results suggest that GIRK channel inhibition may reveal a novel characteristic of the commonly used antidepressants, particularly sertraline, and contributes to some of the therapeutic effects and adverse effects...
  5. pmc Inhibition of G-protein-activated inwardly rectifying K+ channels by the selective norepinephrine reuptake inhibitors atomoxetine and reboxetine
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Chuo Ku, Niigata, Japan
    Neuropsychopharmacology 35:1560-9. 2010
    ..GIRK channel inhibition may contribute to some of the therapeutic effects of NRIs and adverse side effects related to nervous system and heart function...
  6. pmc Pregnenolone sulfate potentiates the inwardly rectifying K channel Kir2.3
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Niigata, Niigata, Japan
    PLoS ONE 4:e6311. 2009
    ..Among constitutively active Kir2 channels in a major Kir subfamily, Kir2.3 channels are expressed predominantly in the forebrain, a brain area related to cognition, memory, emotion, and neuropsychiatric disorders...
  7. doi request reprint Inhibitory effects of the antiepileptic drug ethosuximide on G protein-activated inwardly rectifying K+ channels
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, 1 757 Asahimachi, Chuo Ku, Niigata, Niigata 951 8585, Japan
    Neuropharmacology 56:499-506. 2009
    ..These results suggest that the inhibitory effects of ethosuximide on GIRK channels may affect some of brain, heart and platelet functions...
  8. ncbi request reprint Inhibition by cocaine of G protein-activated inwardly rectifying K+ channels expressed in Xenopus oocytes
    Toru Kobayashi
    Division of Psychobiology, Tokyo Institute of Psychiatry, 2 1 8 Kamikitazawa, Setagaya Ku, Tokyo 156 8585, Japan
    Toxicol In Vitro 21:656-64. 2007
    ..Our results suggest that inhibition of GIRK channels by cocaine may contribute to some of its toxic effects...
  9. ncbi request reprint Inhibition of G protein-activated inwardly rectifying K+ channels by the antidepressant paroxetine
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Niigata, Japan
    J Pharmacol Sci 102:278-87. 2006
    ..Our results suggest that inhibition of GIRK channels by paroxetine may contribute partly to some of its therapeutic effects and adverse side effects...
  10. pmc Functional characterization of an endogenous Xenopus oocyte adenosine receptor
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, 1 757 Asahimachi, Niigata, Niigata 951 8585, Japan
    Br J Pharmacol 135:313-22. 2002
    ....
  11. pmc Inhibition of G protein-activated inwardly rectifying K+ channels by fluoxetine (Prozac)
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, 1 757 Asahimachi, Niigata, Niigata 951 8585, Japan
    Br J Pharmacol 138:1119-28. 2003
    ..The present results suggest that inhibition of GIRK channels by fluoxetine may contribute to some of its therapeutic effects and adverse side effects, particularly seizures in overdose, observed in clinical practice...
  12. ncbi request reprint Inhibition of G protein-activated inwardly rectifying K+ channels by various antidepressant drugs
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Niigata, Japan
    Neuropsychopharmacology 29:1841-51. 2004
    ....
  13. ncbi request reprint Effects of interferon-alpha on cloned opioid receptors expressed in Xenopus oocytes
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, 1 757 Asahimachi, Niigata, Niigata 951 8585, Japan
    Life Sci 76:407-15. 2004
    ..The direct activation of the delta- and kappa-opioid receptors by IFNalpha may partly contribute to some of the IFNalpha effects under its high-dose medication...
  14. ncbi request reprint Inhibition of G protein-activated inwardly rectifying K+ channels by ifenprodil
    Toru Kobayashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Niigata, Japan
    Neuropsychopharmacology 31:516-24. 2006
    ..Our results suggest that direct inhibition of GIRK channels by ifenprodil, at submicromolar concentrations or more, may contribute to some of its therapeutic effects and adverse side effects...
  15. ncbi request reprint G protein-activated inwardly rectifying K+ channel inhibition and rescue of weaver mouse motor functions by antidepressants
    Takehiro Takahashi
    Division of Psychobiology, Tokyo Institute of Psychiatry, 2 1 8 Kamikitazawa Setagaya, Tokyo 156 8585, Japan
    Neurosci Res 54:104-11. 2006
    ..These results provide evidence for in vivo GIRK channel inhibition by a group of antidepressants...
  16. ncbi request reprint Opioid receptor coupling to GIRK channels. In vitro studies using a Xenopus oocyte expression system and in vivo studies on weaver mutant mice
    Kazutaka Ikeda
    Department of Molecular Psychiatry, Tokyo Institute of Psychiatry, Laboratory for Neurobiology of Emotion, RIKEN Brain Science Institute, Japan
    Methods Mol Med 84:53-64. 2003
  17. ncbi request reprint Molecular mechanisms of analgesia induced by opioids and ethanol: is the GIRK channel one of the keys?
    Kazutaka Ikeda
    Department of Molecular Psychiatry, Tokyo Institute of Psychiatry, 2 1 8 Kamikitazawa, Setagaya Ku, Tokyo 156 8585, Japan
    Neurosci Res 44:121-131. 2002
    ..The GIRK channel is potentially one of the key molecules in furthering the understanding of the pain control system and in developing advanced analgesics with fewer adverse effects...
  18. ncbi request reprint Gene expression in the brain from fluoxetine-injected mouse using DNA microarray
    Yasuo Takahashi
    Department of Molecular Neuropathology, Brain Research Institute, Niigata University, Niigata, Japan
    Ann N Y Acad Sci 1074:42-51. 2006
    ..We used DNA microarray method for examining the gene expression in the brain. We found the downregulation of many spot signals in the fluoxetine-treated mouse, for example cholecystockinin and prostaglandin D2 synthase...