ArticlePain2009
Regulation of the trigeminal NR1 subunit expression induced by inflammation of the temporomandibular joint region in rats.
Article in Pain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Inflammation-related collagen fibril destruction contributes to temporomandibular joint disc displacement via NF-κB activation.International journal of oral science · 2025Article
- Pluripotential GluN1 (NMDA NR1): Functional Significance in Cellular Nuclei in Pain/Nociception.International journal of molecular sciences · 2023Review
- Decreased PPARgamma in the trigeminal spinal subnucleus caudalis due to neonatal injury contributes to incision-induced mechanical allodynia in female rats.Scientific reports · 2022Article
- NMDARs mediate peripheral and central sensitization contributing to chronic orofacial pain.Frontiers in cellular neuroscience · 2022Review
- Integrated Analysis of Omics Data Reveal AP-1 as a Potential Regulation Hub in the Inflammation-Induced Hyperalgesia Rat Model.Frontiers in immunology · 2021Article
- Sevoflurane plays a reduced role in cognitive impairment compared with isoflurane: limited effect on fear memory retention.Neural regeneration research · 2020Article
- The dietary constituent resveratrol suppresses nociceptive neurotransmission via the NMDA receptor.Molecular pain · 2017Article
- Kynurenic acid modulates experimentally induced inflammation in the trigeminal ganglion.The journal of headache and pain · 2015Article
- Article
- Brain indoleamine 2,3-dioxygenase contributes to the comorbidity of pain and depression.The Journal of clinical investigation · 2012Article
- The inhalation anesthetic isoflurane increases levels of proinflammatory TNF-α, IL-6, and IL-1β.Neurobiology of aging · 2012Article
- Peripheral N-methyl-d-aspartate receptors contribute to mechanical hypersensitivity in a rat model of inflammatory temporomandibular joint pain.European journal of pain (London, England) · 2011Article
- The role of trigeminal interpolaris-caudalis transition zone in persistent orofacial pain.International review of neurobiology · 2011Review
- Article
- NMDA receptor blockade reduces temporomandibular joint-evoked activity of trigeminal subnucleus caudalis neurons in an estrogen-dependent manner.Neuroscience · 2009Article
- The "toll" of opioid-induced glial activation: improving the clinical efficacy of opioids by targeting glia.Trends in pharmacological sciences · 2009Review
- Microinjection of IL-1β into the trigeminal transition zone produces bilateral NMDA receptor-dependent orofacial hyperalgesia involving descending circuitry.The open pain journal · 2009Article
- Differential expression of connexins in trigeminal ganglion neurons and satellite glial cells in response to chronic or acute joint inflammation.Neuron glia biology · 2008Article
- CXCL12/CXCR4 signaling mediated ERK1/2 activation in spinal cord contributes to the pathogenesis of postsurgical pain in rats.Molecular painArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Expression of the N-methyl-d-aspartate (NMDA) receptor in trigeminal nuclei has been shown to play a role in the mechanisms of trigeminal pain. Here, we examined the hypothesis that the upregulation of the NR1 subunit of the NMDA receptor (NR1) in the trigeminal subnucleus caudalis (Sp5c) following inflammation of the temporomandibular joint (TMJ) region would be regulated by interleukin-6 (IL-6) and the nuclear factor-kappa B (NF-kappaB). Inflammation of a unilateral TMJ region was produced in rats by injecting 50mul of complete Freund's adjuvant (CFA) into a TMJ and adjacent tissues, which resulted in persistent pain behavior as assessed using algometer before (baseline) and on days 1, 3, and 7 after the CFA injection. The CFA injection also induced a significant upregulation of NR1 and NF-kappaB on days 3 and 7, and of IL-6 on days 1, 3, and 7, within the ipsilateral Sp5c, as compared with the sham TMJ injection group. Once daily intracisternal injection of an IL-6 antiserum or NF-kappaB inhibitor (PDTC) for 6 days, beginning on day 1 immediately after the CFA injection, prevented both the upregulation of NR1 in the ipsilateral Sp5C and pain behavior. Moreover, once daily intracisternal IL-6 administration for 6 days in naïve rats induced the NR1 upregulation and pain behavior similar to that after TMJ inflammation. These results indicate that the upregulation of IL-6 and NF-kappaB after inflammation of the unilateral TMJ region is a critical regulatory mechanism for the expression of NR1 in the ipsilateral Sp5c, which contributed to the development of TMJ pain behavior in rats.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.