ArticleJournal of molecular neuroscience : MN2013
Peripheral metabotropic glutamate receptor subtype 5 contributes to inflammation-induced hypersensitivity of the rat temporomandibular joint.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Peripheral role of glutamate in orofacial pain.Frontiers in neuroscience · 2022Review
- Glutamate and Its Receptors as Therapeutic Targets for Migraine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters.Neuroscience letters · 2017Article
- Localization and role of metabotropic glutamate receptors subtype 5 in the gastrointestinal tract.World journal of gastroenterology · 2017Review
- Metabotropic glutamate receptor 5: a target for migraine therapy.Annals of clinical and translational neurology · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
Temporomandibular disorders (TMD) comprise an assortment of clinical conditions characterized by pain in the temporomandibular joint (TMJ). TMD patients have a variety of symptoms, including jaw movement disorder and TMJ pain. Metabotropic glutamate receptor subtype 5 (mGluR5) was reported to be involved in pain processing in several animal models of neuropathic and inflammatory pain. In this study, the head withdrawal threshold and mGluR5 expression were investigated in rats with complete Freund's adjuvant (CFA)-induced TMJ inflammatory pain. CFA injection into the TMJ significantly decreased the mechanical head withdrawal thresholds relative to vehicle injection, and the effects were blocked by pre-injection of 2-methyl-6-(phenylethynyl)-pyridine (MPEP). mGluR5 expression in the trigeminal ganglion was predominantly increased in the CFA-injected group compared with the normal control group. Pretreatment with MPEP, a selective mGluR5 antagonist, reduced mGluR5 expression in the trigeminal ganglion compared with the CFA group, as measured by immunohistochemistry, western blotting, and RT-PCR. Significant differences in the proportion or intensity of mGluR5 expression were found in animals with inflammation versus control animals at the examined time point. These findings indicate a role for peripheral mGluR5 in CFA-induced nociceptive behavior and TMJ inflammation. Peripheral application of mGluR5 antagonists could provide therapeutic benefits for inflammatory TMJ pain.
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