ArticleThe European journal of neuroscience2003
Potentiation of evoked calcitonin gene-related peptide release from oral mucosa: a potential basis for the pro-inflammatory effects of nicotine.
Article in The European journal of neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 50 citations in OpenAlex.
- Chili Pepper Flavourants in "Heat" and "Unflavoured" Oral Nicotine Pouches Marketed in the United States.bioRxiv : the preprint server for biology · 2026Article
- Peripheral Parasympathetic Networks in Pain: A Systems-Level Review of Mechanisms and Modulations.Cellular and molecular neurobiology · 2025Review
- HIV-1 gp120 Interactions with Nicotine Modulate Mitochondrial Network Properties and Amyloid Release in Microglia.Neurochemical research · 2025Article
- Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects.Frontiers in immunology · 2022Review
- Review
- Smoking History and Clinical Features of Cluster Headache: Results from the Korean Cluster Headache Registry.Journal of clinical neurology (Seoul, Korea) · 2021Article
- Comparative Analysis of Dorsal Root, Nodose and Sympathetic Ganglia for the Development of New Analgesics.Frontiers in neuroscience · 2020Article
- To flourish or perish: evolutionary TRiPs into the sensory biology of plant-herbivore interactions.Pflugers Archiv : European journal of physiology · 2019Review
- Ablation of sensory neurons in a genetic model of pancreatic ductal adenocarcinoma slows initiation and progression of cancer.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Prenatal nicotinic exposure upregulates pulmonary C-fiber NK1R expression to prolong pulmonary C-fiber-mediated apneic response.Toxicology and applied pharmacology · 2016Article
- CX3CR1 Mediates Nicotine Withdrawal-Induced Hyperalgesia via Microglial P38 MAPK Signaling.Neurochemical research · 2015Article
- The nicotinic α6 subunit gene determines variability in chronic pain sensitivity via cross-inhibition of P2X2/3 receptors.Science translational medicine · 2015Article
- Prenatal nicotinic exposure augments cardiorespiratory responses to activation of bronchopulmonary C-fibers.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Inflammation-induced increase in nicotinic acetylcholine receptor current in cutaneous nociceptive DRG neurons from the adult rat.Neuroscience · 2015Article
- Molecular signatures of mouse TRPV1-lineage neurons revealed by RNA-Seq transcriptome analysis.The journal of pain · 2014Article
- Artemin growth factor increases nicotinic cholinergic receptor subunit expression and activity in nociceptive sensory neurons.Molecular pain · 2014Article
- Cholinergic neurotransmission links solitary chemosensory cells to nasal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- TRPs in taste and chemesthesis.Handbook of experimental pharmacology · 2014Review
- Nicotine activates the chemosensory cation channel TRPA1.Nature neuroscience · 2009Article
- Impact of chronic nicotine on sciatic nerve injury in the rat.Journal of neuroimmunology · 2007Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Inflammation of the buccal mucosa, gingiva and periodontal tissues is a significant problem in users of nicotine-containing tobacco products; however, the potential role of nicotine in the development of this inflammation is unclear. In many tissues, nicotine, acting through nicotinic acetylcholine receptors (nAChRs), has been shown to increase the release of the pro-inflammatory mediator calcitonin gene-related peptide (CGRP) thereby potentially contributing to neurogenic inflammation. The purpose of the present studies was to determine the effects of nicotine and other nAChR agonists on capsaicin-evoked immunoreactive CGRP (iCGRP) release from rat buccal mucosa and to identify a potential cellular basis for these effects. Using a previously validated model of in vitro superfusion, we show that the nAChR agonists nicotine (EC50 557 micro m), epibatidine (EC50 317 pm) and cytisine (EC50 4.83 nm) potentiated capsaicin-evoked iCGRP release in a concentration-dependent manner by 123, 70 and 76%, respectively. The expression and distribution patterns of the mRNA transcripts encoding the alpha3, alpha4 and alpha6 nAChR subunits and their colocalization with CGRP and the capsaicin receptor VR1 were examined in rat trigeminal ganglion using combined in situ hybridization and immunohistofluorescence. Of all trigeminal neurons counted, mRNA encoding the alpha3, alpha4 and alpha6 subunits was found, respectively, in 14.45, 9.2 and 19.21% of neurons. The cell body diameter of most neurons containing any nAChR subunit was in the 30-40 micro m range with slightly fewer in the 20-30 micro m range. Co-localization of these alpha subunit transcripts with either CGRP or VR1 immunoreactivity ranged from approximately 5 to 7% for alpha4 and over 8% for alpha3 to 18% for alpha6. These data support the hypothesis that nicotinic agents, acting at nAChRs contained on primary sensory neurons, are capable of directly modulating the stimulated release of iCGRP. In the case of users of nicotine-containing tobacco products, this modulation could contribute to inflammatory processes within the oral cavity.
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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.