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Open Access Research

TRPV1 channel-mediated bilateral allodynia induced by unilateral masseter muscle inflammation in rats

Suncana Simonic-Kocijan12, Xuehong Zhao13, Wen Liu1, Yuwei Wu4, Ivone Uhac2 and KeWei Wang156*

Author Affiliations

1 Department of Neurobiology, Neuroscience Research Institute, Peking University Health Science Center, Beijing, China

2 Department of Prosthodontics, School of Dental Medicine, Medical Faculty, Rijeka University, Krešimirova 40, 51000, Rijeka, Croatia

3 Medical function Department, Medical College of Hubei University of Arts and Science, Xiangyang 441053, China

4 The 2nd Dental Center, Peking University School of Stomatology, 38 Xueyuan Road, Beijing 100191, China

5 Department of Molecular and Cellular Pharmacology, Peking University School of Pharmaceutical Sciences, 38 Xueyuan Road, Beijing 100191, China

6 PKU-IDG/McGovern Institute for Brain Research, Peking University, Beijing 100871, China

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Molecular Pain 2013, 9:68  doi:10.1186/1744-8069-9-68

Published: 30 December 2013


Pain in masticatory muscles is among the most prominent symptoms of temperomandibular disorders (TMDs) that have diverse and complex etiology. A common complaint of TMD is that unilateral pain of craniofacial muscle can cause a widespread of bilateral pain sensation, although the underlying mechanism remains unknown. To investigate whether unilateral inflammation of masseter muscle can cause a bilateral allodynia, we generated masseter muscle inflammation induced by unilateral injection of complete Freund’s adjuvant (CFA) in rats, and measured the bilateral head withdrawal threshold at different time points using a von Frey anesthesiometer. After behavioral assessment, both right and left trigeminal ganglia (TRG) were dissected and examined for histopathology and transient receptor potential vanilloid 1 (TRPV1) mRNA expression using quantitative real-time PCR analysis. A significant increase in TRPV1 mRNA expression occurred in TRG ipsilateral to CFA injected masseter muscle, whereas no significant alteration in TRPV1 occurred in the contralateral TRG. Interestingly, central injection of TRPV1 antagonist 5-iodoresiniferatoxin into the hippocampus significantly attenuated the head withdrawal response of both CFA injected and non-CFA injected contralateral masseter muscle. Our findings show that unilateral inflammation of masseter muscle is capable of inducing bilateral allodynia in rats. Upregulation of TRPV1 at the TRG level is due to nociception caused by inflammation, whereas contralateral nocifensive behavior in masticatory muscle nociception is likely mediated by central TRPV1, pointing to the involvement of altered information processing in higher centers.

Hippocampus; Masseter muscle; TMD; TRG; TRPV1