ArticleJournal of oral & facial pain and headache
Central Role of Protein Kinase A in Promoting Trigeminal Nociception in an In Vivo Model of Temporomandibular Disorders.
Article in Journal of oral & facial pain and headache. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Up-regulation of peripheral and central CGRP expression combined with subchondral bone remodeling in rat MIA-induced TMJOA model.Journal of oral & facial pain and headache · 2025Article
- Preclinical perspectives on disorders of the temporomandibular joint: Tracing the past, navigating the present, and shaping the future.The journal of pain · 2025Review
- Desloratadine ameliorates paclitaxel-induced peripheral neuropathy and hypersensitivity reactions in mice.Acta pharmacologica Sinica · 2024Article
- Sensory Neuron-TRPV4 Modulates Temporomandibular Disorder Pain Via CGRP in Mice.The journal of pain · 2023Review
- Glia and Orofacial Pain: Progress and Future Directions.International journal of molecular sciences · 2021Review
- Neuromedin B receptor stimulation of Cav3.2 T-type CaTheranostics · 2021Article
- The effectiveness of photobiomodulation in the management of temporomandibular pain sensitivity in rats: behavioral and neurochemical effects.Lasers in medical science · 2020Article
- The Role of Nociceptive Neurons in the Pathogenesis of Psoriasis.Frontiers in immunology · 2020Review
- Secondary traumatic stress increases expression of proteins implicated in peripheral and central sensitization of trigeminal neurons.Brain research · 2018Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
aimsTo investigate cellular changes in the spinal trigeminal nucleus (STN) and trigeminal ganglion (TG) associated with trigeminal nociception mediated by inflammation in the temporomandibular joint (TMJ).
methodsMale Sprague-Dawley rats (n = 86) were utilized to investigate cellular and behavioral responses to prolonged TMJ inflammation caused by bilateral injection of Complete Freund's Adjuvant (CFA) in the TMJ capsules. To investigate the cellular effects of protein kinase A (PKA) in the STN, rats were injected intrathecally with the selective PKA inhibitor KT5720 prior to injection of CFA into both TMJ capsules. Levels of calcitonin gene-related peptide (CGRP), active PKA, and ionized calcium-binding adapter molecule 1 (Iba1) in the STN and expression of phosphorylated extracellular regulated kinases (p-ERK) in the TG were determined with immunohistochemistry (n ≥ 3 experiments per test condition). Nocifensive head withdrawal responses to mechanical stimulation of the cutaneous tissue over the TMJ were monitored following CFA injection in the absence or presence of KT5720 (n = 7). Statistical analysis was performed using parametric analysis of variance (ANOVA) tests.
resultsIntrathecal injection of KT5720 significantly inhibited the stimulatory effect of CFA on levels of CGRP, PKA, and Iba1 in the STN. In addition, administration of KT5720 decreased the average number of CFA-induced nocifensive withdrawal responses to mechanical stimulation and the CFA-mediated increase in p-ERK expression in the ganglion.
conclusionThese findings provide evidence that elevated PKA activity in the STN promotes cellular events temporally associated with trigeminal nociception caused by prolonged TMJ inflammation.
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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.