M Takeda

Summary

Affiliation: The Nippon Dental University
Country: Japan

Publications

  1. Takeda M, Takahashi M, Matsumoto S. Contribution of activated interleukin receptors in trigeminal ganglion neurons to hyperalgesia via satellite glial interleukin-1beta paracrine mechanism. Brain Behav Immun. 2008;22:1016-23 pubmed publisher
    ..Such an IL-1beta release could be important in determining trigeminal inflammatory hyperalgesia. ..
  2. Takeda M, Kitagawa J, Nasu M, Takahashi M, Iwata K, Matsumoto S. Glial cell line-derived neurotrophic factor acutely modulates the excitability of rat small-diameter trigeminal ganglion neurons innervating facial skin. Brain Behav Immun. 2010;24:72-82 pubmed publisher
    ..We therefore conclude that a local release of GDNF from TRG neuronal soma and/or nerve terminals may regulate normal sensory function, including nociception. ..
  3. Takeda M, Takahashi M, Hara N, Matsumoto S. Glial cell line-derived neurotrophic factor modulates the excitability of nociceptive trigeminal ganglion neurons via a paracrine mechanism following inflammation. Brain Behav Immun. 2013;28:100-7 pubmed publisher
    ..GDNF paracrine mechanism could be important as a therapeutic target for trigeminal inflammatory hyperalgesia. ..
  4. request reprint
    Takeda M, Tanimoto T, Nishikawa T, Ikeda M, Yoshida S, Ito M, et al. Volume expansion suppresses the tooth-pulp evoked jaw-opening reflex related activity of trigeminal neurons in rats. Brain Res Bull. 2002;58:83-9 pubmed
    ..These results therefore suggest that low-pressure cardiopulmonary baroreceptors whose afferents travel in the vagus nerve inhibit the pulpal nociceptive transmission. ..
  5. Takeda M, Kitagawa J, Takahashi M, Matsumoto S. Activation of interleukin-1beta receptor suppresses the voltage-gated potassium currents in the small-diameter trigeminal ganglion neurons following peripheral inflammation. Pain. 2008;139:594-602 pubmed publisher
    ..These findings provide evidence for the development of voltage-gated K(+) channel openers and IL-1beta antagonists as therapeutic agents for the treatment of trigeminal inflammatory hyperalgesia. ..
  6. request reprint
    Takeda M, Tanimoto T, Ito M, Nasu M, Matsumoto S. Role of capsaicin-sensitive primary afferent inputs from the masseter muscle in the C1 spinal neurons responding to tooth-pulp stimulation in rats. Exp Brain Res. 2005;160:107-17 pubmed
    ....
  7. request reprint
    Takeda M, Tanimoto T, Ikeda M, Nasu M, Kadoi J, Yoshida S, et al. Enhanced excitability of rat trigeminal root ganglion neurons via decrease in A-type potassium currents following temporomandibular joint inflammation. Neuroscience. 2006;138:621-30 pubmed
    ..These changes may contribute to trigeminal inflammatory allodynia in temporomandibular joint disorder...
  8. request reprint
    Takeda M, Tanimoto T, Nasu M, Matsumoto S. Temporomandibular joint inflammation decreases the voltage-gated K+ channel subtype 1.4-immunoreactivity of trigeminal ganglion neurons in rats. Eur J Pain. 2008;12:189-95 pubmed
    ..These results lead us to suggest that Kv channel openers may be a potential therapeutic agents for prevention of mechanical allodynia. ..
  9. request reprint
    Takeda M, Kadoi J, Takahashi M, Nasu M, Matsumoto S. Somatostatin inhibits the excitability of rat small-diameter trigeminal ganglion neurons that innervate nasal mucosa and project to the upper cervical dorsal horn via activation of somatostatin 2a receptor. Neuroscience. 2007;148:744-56 pubmed
    ....
  10. Takeda M, Takahashi M, Nasu M, Matsumoto S. Peripheral inflammation suppresses inward rectifying potassium currents of satellite glial cells in the trigeminal ganglia. Pain. 2011;152:2147-56 pubmed publisher
    ..Therefore, the Kir4.1 channel in SGCs may be a new molecular target for the treatment of trigeminal inflammatory pain. ..

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Collaborators

Detail Information

Publications10

  1. Takeda M, Takahashi M, Matsumoto S. Contribution of activated interleukin receptors in trigeminal ganglion neurons to hyperalgesia via satellite glial interleukin-1beta paracrine mechanism. Brain Behav Immun. 2008;22:1016-23 pubmed publisher
    ..Such an IL-1beta release could be important in determining trigeminal inflammatory hyperalgesia. ..
  2. Takeda M, Kitagawa J, Nasu M, Takahashi M, Iwata K, Matsumoto S. Glial cell line-derived neurotrophic factor acutely modulates the excitability of rat small-diameter trigeminal ganglion neurons innervating facial skin. Brain Behav Immun. 2010;24:72-82 pubmed publisher
    ..We therefore conclude that a local release of GDNF from TRG neuronal soma and/or nerve terminals may regulate normal sensory function, including nociception. ..
  3. Takeda M, Takahashi M, Hara N, Matsumoto S. Glial cell line-derived neurotrophic factor modulates the excitability of nociceptive trigeminal ganglion neurons via a paracrine mechanism following inflammation. Brain Behav Immun. 2013;28:100-7 pubmed publisher
    ..GDNF paracrine mechanism could be important as a therapeutic target for trigeminal inflammatory hyperalgesia. ..
  4. request reprint
    Takeda M, Tanimoto T, Nishikawa T, Ikeda M, Yoshida S, Ito M, et al. Volume expansion suppresses the tooth-pulp evoked jaw-opening reflex related activity of trigeminal neurons in rats. Brain Res Bull. 2002;58:83-9 pubmed
    ..These results therefore suggest that low-pressure cardiopulmonary baroreceptors whose afferents travel in the vagus nerve inhibit the pulpal nociceptive transmission. ..
  5. Takeda M, Kitagawa J, Takahashi M, Matsumoto S. Activation of interleukin-1beta receptor suppresses the voltage-gated potassium currents in the small-diameter trigeminal ganglion neurons following peripheral inflammation. Pain. 2008;139:594-602 pubmed publisher
    ..These findings provide evidence for the development of voltage-gated K(+) channel openers and IL-1beta antagonists as therapeutic agents for the treatment of trigeminal inflammatory hyperalgesia. ..
  6. request reprint
    Takeda M, Tanimoto T, Ito M, Nasu M, Matsumoto S. Role of capsaicin-sensitive primary afferent inputs from the masseter muscle in the C1 spinal neurons responding to tooth-pulp stimulation in rats. Exp Brain Res. 2005;160:107-17 pubmed
    ....
  7. request reprint
    Takeda M, Tanimoto T, Ikeda M, Nasu M, Kadoi J, Yoshida S, et al. Enhanced excitability of rat trigeminal root ganglion neurons via decrease in A-type potassium currents following temporomandibular joint inflammation. Neuroscience. 2006;138:621-30 pubmed
    ..These changes may contribute to trigeminal inflammatory allodynia in temporomandibular joint disorder...
  8. request reprint
    Takeda M, Tanimoto T, Nasu M, Matsumoto S. Temporomandibular joint inflammation decreases the voltage-gated K+ channel subtype 1.4-immunoreactivity of trigeminal ganglion neurons in rats. Eur J Pain. 2008;12:189-95 pubmed
    ..These results lead us to suggest that Kv channel openers may be a potential therapeutic agents for prevention of mechanical allodynia. ..
  9. request reprint
    Takeda M, Kadoi J, Takahashi M, Nasu M, Matsumoto S. Somatostatin inhibits the excitability of rat small-diameter trigeminal ganglion neurons that innervate nasal mucosa and project to the upper cervical dorsal horn via activation of somatostatin 2a receptor. Neuroscience. 2007;148:744-56 pubmed
    ....
  10. Takeda M, Takahashi M, Nasu M, Matsumoto S. Peripheral inflammation suppresses inward rectifying potassium currents of satellite glial cells in the trigeminal ganglia. Pain. 2011;152:2147-56 pubmed publisher
    ..Therefore, the Kir4.1 channel in SGCs may be a new molecular target for the treatment of trigeminal inflammatory pain. ..