ArticleNeuroscience2008
Nitric oxide-proton stimulation of trigeminal ganglion neurons increases mitogen-activated protein kinase and phosphatase expression in neurons and satellite glial cells.
Article in Neuroscience, 2008. 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, 38 citations in OpenAlex.
- Neuroimmune alterations and nociceptive behavior in oral carcinogenesis in rats.European journal of oral sciences · 2026Article
- Various gases for the treatment of neuropathic pain: mechanisms, current status, and future perspectives.Medical gas research · 2025Review
- Changes of Trigeminal Ganglion Neurons Innervating the Temporomandibular Joint in Chronic Pain Rat Model.International journal of dentistry · 2024Article
- The degeneration-pain relationship in the temporomandibular joint: Current understandings and rodent models.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Grape seed extract suppresses calcitonin gene-related peptide secretion and upregulates expression of GAD 65/67 and GABAB receptor in primary trigeminal ganglion cultures.IBRO neuroscience reports · 2022Article
- Peripheral and Central Mechanisms of Persistent Orofacial Pain.Frontiers in neuroscience · 2019Review
- Secondary traumatic stress increases expression of proteins implicated in peripheral and central sensitization of trigeminal neurons.Brain research · 2018Article
- Tetrandrine Alleviates Nociception in a Rat Model of Migraine via Suppressing S100B and p-ERK Activation in Satellite Glial Cells of the Trigeminal Ganglia.Journal of molecular neuroscience : MN · 2018Article
- Vagus nerve stimulation inhibits trigeminal nociception in a rodent model of episodic migraine.Pain reports · 2017Article
- Diverse Physiological Roles of Calcitonin Gene-Related Peptide in Migraine Pathology: Modulation of Neuronal-Glial-Immune Cells to Promote Peripheral and Central Sensitization.Current pain and headache reports · 2016Review
- Kynurenic acid modulates experimentally induced inflammation in the trigeminal ganglion.The journal of headache and pain · 2015Article
- Dural administration of inflammatory soup or Complete Freund's Adjuvant induces activation and inflammatory response in the rat trigeminal ganglion.The journal of headache and pain · 2015Article
- Mitogen-Activated Protein Kinase Phosphatase (MKP)-1 in Nervous System Development and Disease.Molecular neurobiology · 2015Review
- Glia and pain: is chronic pain a gliopathy?Pain · 2013Review
- Spinal mitogen-activated protein kinase phosphatase-3 (MKP-3) is necessary for the normal resolution of mechanical allodynia in a mouse model of acute postoperative pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Exploring the neuroimmunopharmacology of opioids: an integrative review of mechanisms of central immune signaling and their implications for opioid analgesia.Pharmacological reviews · 2011Review
- Development of functional units within trigeminal ganglia correlates with increased expression of proteins involved in neuron-glia interactions.Neuron glia biology · 2010Article
- Proinflammatory-activated trigeminal satellite cells promote neuronal sensitization: relevance for migraine pathology.Molecular pain · 2009Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Elevated nitric oxide (NO) and proton levels in synovial fluid are implicated in joint pathology. However, signaling pathways stimulated by these molecules that mediate inflammation and pain in the temporomandibular joint (TMJ) have not been investigated. The goal of this study was to determine the effect of NO-proton stimulation of rat trigeminal neurons on the in vivo expression of mitogen-activated protein kinases (MAPKs) and phosphatases (MKPs) in trigeminal ganglion neurons and satellite glial cells. Low levels of the active MAPKs extracellular signal-regulated kinase (ERK), Jun amino-terminal kinase (JNK), and p38 were localized in the cytosol of neurons and satellite glial cells in unstimulated animals. However, increased levels of active ERK and p38, but not JNK, were detected in the cytosol and nucleus of V3 neurons and satellite glial cells 15 min and 2 h following bilateral TMJ injections of an NO donor diluted in pH 5.5 medium. While ERK levels returned to near basal levels 24 h after stimulation, p38 levels remained significantly elevated. In contrast to MKP-2 and MKP-3 levels that were barely detectable in neurons or satellite glial cells, MKP-1 staining was readily observed in satellite glial cells in ganglia from unstimulated animals. However, neuronal and satellite glial cell staining for MKP-1, MKP-2, and MKP-3 was significantly increased in response to NO-protons. Increased active ERK and p38 levels as well as elevated MKP levels were also detected in neurons and satellite glial cells located in V2 and V1 regions of the ganglion. Our data provide evidence that NO-proton stimulation of V3 neurons results in temporal and spatial changes in expression of active ERK and p38 and MKPs in all regions of the ganglion. We propose that in trigeminal ganglia these cellular events, which are involved in peripheral sensitization as well as control of inflammatory and nociceptive responses, may play a role in TMJ pathology.
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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.