PMID- 25741041
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 0027-7622 (Print)
IS  - 2186-3326 (Electronic)
IS  - 0027-7622 (Linking)
VI  - 76
IP  - 3-4
DP  - 2014 Aug
TI  - Involvement of glial activation in trigeminal ganglion in a rat model of lower 
      gingival cancer pain.
PG  - 323-32
AB  - Glial cells were investigated to elucidate their involvement in mechanisms 
      underlying oral cancer pain. Squamous cell carcinoma (SCC-158) was inoculated 
      into the lower gingiva of male Fisher rats. Pharmacological and 
      immunohistochemical studies were performed to examine the roles played by TRPV1 
      and TRPV2 expressed in neurons and satellite glia in trigeminal ganglia (TG), and 
      microglia and astrocytes in trigeminal spinal nucleus caudalis. Inoculation of 
      SCC-158 into the lower gingiva induced marked mechanical allodynia in the 
      whisker-pad skin area on days 16 through 28, and in the submandibular skin area 
      on days 10 through 20. Cutaneous allodynia was diminished by systemic morphine 
      administration. The number of TRPV1 and TRPV2-positive neurons in trigeminal 
      ganglia increased in the medium and large cell groups on day 14 after tumor 
      inoculation. The number of satellite glial cells encircling the medium and large 
      trigeminal ganglion neurons increased on day 28 after tumor inoculation. In this 
      gingival cancer pain model, microglia and astrocytes in trigeminal spinal nucleus 
      caudalis were not activated, although they were reported to be activated in 
      neuropathic and inflammatory pain models. These results suggest that TRPV1 and 
      TRPV2 upregulation in trigeminal ganglion neurons may play an important role in 
      inducing the mechanical allodynia observed in experimental models of oral 
      squamous cell carcinoma. In addition, activation of satellite cells seems to be 
      involved in the maintenance of mechanical allodynia, which could be the potential 
      therapeutic target for oral cancer pain.
FAU - Hironaka, Katsunori
AU  - Hironaka K
AD  - Department of Oral and Maxillofacial Surgery, Nagoya University Graduate School 
      of Medicine, Nagoya, Japan ; Department of Functional Anatomy and Neuroscience, 
      Nagoya University Graduate School of Medicine, Nagoya, Japan.
FAU - Ozaki, Noriyuki
AU  - Ozaki N
AD  - Department of Functional Anatomy, Kanazawa University Graduate School of Medical 
      Science, Kanazawa, Japan.
FAU - Hattori, Hisashi
AU  - Hattori H
AD  - Department of Oral and Maxillofacial Surgery, Nagoya University Graduate School 
      of Medicine, Nagoya, Japan.
FAU - Nagamine, Kenjiro
AU  - Nagamine K
AD  - Department of Oral and Maxillofacial Surgery, Nagoya University Graduate School 
      of Medicine, Nagoya, Japan.
FAU - Nakashima, Hideyuki
AU  - Nakashima H
AD  - Department of Oral and Maxillofacial Surgery, Nagoya University Graduate School 
      of Medicine, Nagoya, Japan.
FAU - Ueda, Minoru
AU  - Ueda M
AD  - Department of Oral and Maxillofacial Surgery, Nagoya University Graduate School 
      of Medicine, Nagoya, Japan.
FAU - Sugiura, Yasuo
AU  - Sugiura Y
AD  - School of Human Care, Nagoya University of Art and Sciences, Nisshin, Japan.
LA  - eng
PT  - Journal Article
PL  - Japan
TA  - Nagoya J Med Sci
JT  - Nagoya journal of medical science
JID - 0412011
SB  - IM
PMC - PMC4345692
OTO - NOTNLM
OT  - GFAP
OT  - Hyperalgesia
OT  - Oral cancer
OT  - TRPV1
OT  - TRPV2
EDAT- 2015/03/06 06:00
MHDA- 2015/03/06 06:01
PMCR- 2014/08/01
CRDT- 2015/03/06 06:00
PHST- 2014/04/07 00:00 [received]
PHST- 2014/07/15 00:00 [accepted]
PHST- 2015/03/06 06:00 [entrez]
PHST- 2015/03/06 06:00 [pubmed]
PHST- 2015/03/06 06:01 [medline]
PHST- 2014/08/01 00:00 [pmc-release]
PST - ppublish
SO  - Nagoya J Med Sci. 2014 Aug;76(3-4):323-32.