Differential Changes in TRPV1 expression after trigeminal sensory nerve injury.
We have recently demonstrated that inferior alveolar nerve and mental nerve (branches of the mandibular nerve) injury from rats serves as a valid trigeminal neuropathic pain model. In these animals, we found that neuronal loss of trigeminal ganglion (TG) was not correlated with pain hypersensitivity. In this study, we examined changes of transient receptor potential vanilloid 1 (TRPV1) expression in the injured and uninjured TG neurons using immunohistochemical analysis at 3 days after surgery, the time point where we observed significant pain hypersensitivity. Injured neurons were identified by positive immunoreactivity for activating transcription factor 3 (ATF3). ATF3 immunoreactivity was exclusively observed in the nuclei of subpopulation of ipsilateral mandibular TG neurons, whereas no ATF3 expression was found in the naive and contralateral TG neurons. Interestingly, the expression of TRPV1 was increased in the uninjured ipsilateral maxillary TG neurons as well as in the uninjured ipsilateral mandibular TG neurons. The upregulation of TRPV1 and ATF3 expression returned to the basal level at 60 days after surgery. Our results demonstrate that trigeminal sensory nerve injury induced differential changes in TRPV1 expression of the injured and uninjured TG neurons. The upregulation of TRPV1 in uninjured TG neurons may play an important role in pain hypersensitivity after trigeminal nerve injury.


CONCLUSIONS
The TRPV1 is a well-known pain transducer molecule and plays crucial roles in the perception of inflammatory and thermal pain. This article presents that TRPV1 expression was increased in uninjured neurons rather than injured neurons after peripheral nerve injury. The upregulation of TRPV1 in uninjured neurons may be associated with the development of neuropathic pain. TRPV1 might be a potential target for the treatment of neuropathic pain.
Kim
Hyun Yeong
HY
Department of Physiology and Program in Molecular and Cellular Neuroscience, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, Korea.
Park
Chul-Kyu
CK
Cho
Ik-Hyun
IH
Jung
Sung Jun
SJ
Kim
Joong Soo
JS
Oh
Seog Bae
SB
D051700:Activating Transcription Factor 3 / Q000378:metabolism; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D002452:Cell Count; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000502:physiology*; D008297:Male; D009474:Neurons / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D050916:TRPV Cation Channels / Q000235:genetics / Q000378:metabolism*; D013997:Time Factors; D012668:Trigeminal Ganglion / Q000473:pathology*; D020433:Trigeminal Nerve Diseases / Q000378:metabolism* / Q000473:pathology
D051700:Activating Transcription Factor 3; D000596:Amino Acids; C497108:Atf3 protein, rat; D050916:TRPV Cation Channels; C493922:Trpv1 protein, rat; C098463:dolaisoleucine