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Involvement of mGluR5 and TRPV1 in visceral nociception in a rat model of uterine cervical distension

Metabotropic glutamate receptor 5 (mGluR5) and transient receptor potential vanilloid subtype 1 (TRPV1) have been shown to play critical roles in the transduction and modulation of cutaneous nociception in the central nervous system. However, little is known regarding the possible involvement of mGl...

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Detalles Bibliográficos
Autores principales: Zhang, Wenxin, Drzymalski, Dan, Sun, Lihong, Xu, Qi, Jiao, Cuicui, Wang, Luyang, Xie, Shufang, Qian, Xiaowei, Wu, Hui, Xiao, Fei, Fu, Feng, Feng, Ying, Chen, Xinzhong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302284/
https://www.ncbi.nlm.nih.gov/pubmed/30444177
http://dx.doi.org/10.1177/1744806918816850
Descripción
Sumario:Metabotropic glutamate receptor 5 (mGluR5) and transient receptor potential vanilloid subtype 1 (TRPV1) have been shown to play critical roles in the transduction and modulation of cutaneous nociception in the central nervous system. However, little is known regarding the possible involvement of mGluR5 and TRPV1 in regulating visceral nociception from the uterine cervix. In this study, we used a rat model of uterine cervical distension to examine the effects of noxious stimuli to the uterine cervix on expression of spinal mGluR5 and TRPV1. Our findings included the following: (1) uterine cervical distension resulted in a stimulus-dependent increase in electromyographic, spinal c-Fos signal, and expression of mGluR5 and TRPV1 in the spinal cord; (2) intrathecal administration of the mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyri-dine significantly reduced the increased TRPV1 and c-Fos expression induced by uterine cervical distension; (3) the TRPV1 inhibitor SB-366791 inhibited increased spinal c-Fos expression but had no effect on the expression of mGluR5 in response to uterine cervical distension. Our findings indicate that the spinal mGluR5-TRPV1 pathway modulates nociceptive transmission in uterine cervical distension-induced pathological visceral pain.