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演題詳細

Poster

痛覚、痒み、及びその障害
Pain, Itch and Their Disorders

開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

咬筋炎症に伴う三叉神経脊髄路中間・尾側亜核境界領域に投射する小型三叉神経節ニューロン興奮性のBDNFによる増強効果 -
BDNF enhances the excitability of small-diameter trigeminal ganglion neurons projecting to the trigeminal nucleus interpolaris/caudalis transition zone following masseter muscle inflammation

  • P2-184
  • 武田 守 / Mamoru Takeda:1 高橋 誠之 / Masayuki Takahashi:2 北川 純一 / Junichi Kitagawa:4 那須 優則 / Masanori Nasu:3 金澤 卓也 / Takuya Kanazawa:2 島津 徳人 / Yoshihito Shimazu:1 松本 茂二 / Shigeji Matsumoto:2 
  • 1:麻布大・生命環境・食品生命・食品生理 / Lab Food Physiol Sci, Dep Food Env Sci, Sch Life Env, Azabu Univ. 2:日本歯大・生命歯・生理 / Dep Physiol, Sch Life Dent, Nippon Dent Univ, Tokyo, Japn 3:日本歯大・生命歯・共同研 / Res Cent Odont, Sch Life Dent, Nippon Dent Univ, Tokyo, Japan 4:新大院医歯・摂食環境・口腔生理 / Div Oral Physiol, Dep Oral Biol Sci, Niigata Univ Grad Sch Med Dent Sci, Niigata, Japan 

The trigeminal subnuclei interpolaris/caudalis transition zones (Vi/Vc) play an important role in orofacial deep pain, however, the role of primary afferent projections to the Vi/Vc remains to be determined.This study investigated the functional significance of hyperalgesia to the brain-derived neurotrophic factor (BDNF)-tyrosine kinase B (trkB) signaling system in trigeminal ganglion (TRG) neurons projecting to the trigeminal nucleus interpolaris/caudalis (Vi/Vc) transition zone following masseter muscle (MM) inflammation. Fluorogold (FG) labeling was used to identify the TRG neurons innervating the MM, while microbeads (MB) were used to label neurons projecting to the Vi/Vc region. FG/MB-labeled TRG neurons were immunoreactive (IR) for BDNF and trkB. The mean number of BDNF/trkB-IR small/medium-diameter TRG neurons was significantly higher in inflamed rats than in naïve rats. In whole-cell current-clamp experiments, the majority of dissociated small-diameter TRG neurons showed a depolarization response to BDNF that was associated with spike discharge, and the concentration of BDNF that evoked a depolarizing response was significantly lower in the inflamed rats. In addition, the relative number of BDNF-induced spikes during current injection was significantly higher in inflamed rats. The BDNF-induced changes in TRG neuron excitability was abolished by tyrosine kinase inhibitor, K252a. The present study provided evidence that BDNF enhances the excitability of the small-diameter TRG neurons projecting onto the Vi/Vc following MM inflammation. These findings suggest that ganglionic BDNF-trkB signaling is a therapeutic target for the treatment of trigeminal inflammatory hyperalgesia.

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