PMID- 24073832
OWN - NLM
STAT- MEDLINE
DCOM- 20140717
LR  - 20220330
IS  - 1744-8069 (Electronic)
IS  - 1744-8069 (Linking)
VI  - 9
DP  - 2013 Sep 30
TI  - Brain-derived neurotrophic factor enhances the excitability of small-diameter 
      trigeminal ganglion neurons projecting to the trigeminal nucleus 
      interpolaris/caudalis transition zone following masseter muscle inflammation.
PG  - 49
LID - 10.1186/1744-8069-9-49 [doi]
AB  - BACKGROUND: 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 Vi/Vc transition zone 
      following masseter muscle (MM) inflammation. RESULTS: The escape threshold from 
      mechanical stimulation applied to skin above the inflamed MM was significantly 
      lower than in naive rats. 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 naive 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. CONCLUSION: 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.
FAU - Takeda, Mamoru
AU  - Takeda M
AD  - Department of Physiology, School of Life Dentistry at Tokyo, Nippon Dental 
      University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo 102-8159, Japan. 
      m-takeda@tokyo.ndu.ac.jp.
FAU - Takahashi, Masayuki
AU  - Takahashi M
FAU - Kitagawa, Junichi
AU  - Kitagawa J
FAU - Kanazawa, Takuya
AU  - Kanazawa T
FAU - Nasu, Masanori
AU  - Nasu M
FAU - Matsumoto, Shigeji
AU  - Matsumoto S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130930
PL  - United States
TA  - Mol Pain
JT  - Molecular pain
JID - 101242662
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Carbazoles)
RN  - 0 (Indole Alkaloids)
RN  - 97161-97-2 (staurosporine aglycone)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Carbazoles/pharmacology
MH  - Indole Alkaloids/pharmacology
MH  - Male
MH  - Masseter Muscle/*metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Trigeminal Ganglion/*drug effects/*metabolism
MH  - Trigeminal Nuclei/*drug effects/*metabolism
PMC - PMC3849633
EDAT- 2013/10/01 06:00
MHDA- 2014/07/18 06:00
PMCR- 2013/09/30
CRDT- 2013/10/01 06:00
PHST- 2013/07/19 00:00 [received]
PHST- 2013/09/24 00:00 [accepted]
PHST- 2013/10/01 06:00 [entrez]
PHST- 2013/10/01 06:00 [pubmed]
PHST- 2014/07/18 06:00 [medline]
PHST- 2013/09/30 00:00 [pmc-release]
AID - 1744-8069-9-49 [pii]
AID - 10.1186/1744-8069-9-49 [doi]
PST - epublish
SO  - Mol Pain. 2013 Sep 30;9:49. doi: 10.1186/1744-8069-9-49.