ArticleHeadache
Effect of carbon dioxide on calcitonin gene-related peptide secretion from trigeminal neurons.
Article in Headache. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Trial
- Improved pharmacokinetics of sumatriptan with Breath Powered™ nasal delivery of sumatriptan powder.Headache · 2013Trial
- No relevant modulation of TRPV1-mediated trigeminal pain by intranasal carbon dioxide in healthy humans.The journal of headache and pain · 2013Trial
- Calcitonin gene-related peptide differentially modulates intracellular calcium levels in response to depolarizing stimuli in trigeminal ganglion neurons and glial cells.Neuroscience · 2025Article
- Poly-IC Alleviates Nitroglycerin-Induced Migraine by Inhibiting Neuroinflammation via TLR3/TRIF Signaling Pathway.CNS neuroscience & therapeutics · 2025Article
- Functional Analysis of TRPA1, TRPM3, and TRPV1 Channels in Human Dermal Arteries and Their Role in Vascular Modulation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- The role of nociceptive neurons in allergic rhinitis.Frontiers in immunology · 2024Review
- Novel Therapeutic Targets for Migraine.Biomedicines · 2023Review
- Peripheral and Central Mechanisms of Persistent Orofacial Pain.Frontiers in neuroscience · 2019Review
- Current and Innovative Pharmacological Options to Treat Typical and Atypical Trigeminal Neuralgia.Drugs · 2018Review
- 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
- Slow Internal Dynamics and Charge Expansion in the Disordered Protein CGRP: A Comparison with Amylin.Biophysical journal · 2015Article
- Review
- Hydrogen sulphide-mediated vasodilatation involves the release of neurotransmitters from sensory nerves in pressurized mesenteric small arteries isolated from rats.British journal of pharmacology · 2013Article
- Two mechanisms involved in trigeminal CGRP release: implications for migraine treatment.Headache · 2013Article
- Neurogenic inflammation: a study of rat trigeminal ganglion.The journal of headache and pain · 2010Article
- Trigeminal antihyperalgesic effect of intranasal carbon dioxide.Life sciences · 2010Article
- Pharmacology.Handbook of clinical neurology · 2010Article
- Nitric oxide-proton stimulation of trigeminal ganglion neurons increases mitogen-activated protein kinase and phosphatase expression in neurons and satellite glial cells.Neuroscience · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe goal of this study was to determine whether the physiological effects of carbon dioxide (CO(2)) involve regulation of CGRP secretion from trigeminal sensory neurons.
backgroundThe neuropeptide calcitonin gene-related peptide (CGRP) is implicated in the pathophysiology of allergic rhinosinusitis and migraine. Recent clinical evidence supports the use of noninhaled intranasal delivery of 100% CO(2) for treatment of these diseases. Patients report 2 distinct physiological events: first, a short duration stinging or burning sensation within the nasal mucosa, and second, alleviation of primary symptoms.
methodsPrimary cultures of rat trigeminal ganglia were utilized to investigate the effects of CO(2) on CGRP release stimulated by a depolarizing stimulus (KCl), capsaicin, nitric oxide, and/or protons. The amount of CGRP secreted into the culture media was determined using a CGRP-specific radioimmunoassay. Intracellular pH and calcium levels were measured in cultured trigeminal neurons in response to CO(2) and stimulatory agents using fluorescent imaging techniques.
resultsIncubation of primary trigeminal ganglia cultures at pH 6.0 or 5.5 was shown to significantly stimulate CGRP release. Similarly, CO(2) treatment of cultures caused a time-dependent acidification of the media, achieving pH values of 5.5-6 that stimulated CGRP secretion. In addition, KCl, capsaicin, and a nitric oxide donor also caused a significant increase in CGRP release. Interestingly, CO(2) treatment of cultures under isohydric conditions, which prevents extracellular acidification while allowing changes in PCO(2) values, significantly repressed the stimulatory effects of KCl, capsaicin, and nitric oxide on CGRP secretion. We found that CO(2) treatment under isohydric conditions resulted in a decrease in intracellular pH and inhibition of the KCl- and capsaicin-mediated increases in intracellular calcium.
conclusionsResults from this study provide the first evidence of a unique regulatory mechanism by which CO(2) inhibits sensory nerve activation, and subsequent neuropeptide release. Furthermore, the observed inhibitory effect of CO(2) on CGRP secretion likely involves modulation of calcium channel activity and changes in intracellular pH.
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