ArticleBrain research2008
Calcitonin gene-related peptide stimulation of nitric oxide synthesis and release from trigeminal ganglion glial cells.
Article in Brain research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 177 citations in OpenAlex.
- A systematic literature review on the role of glial cells in the pathomechanisms of migraine.Frontiers in molecular neuroscience · 2023Pooled it
- Article
- A delayed endothelial-glial mechanism for CGRP-induced migraine.The journal of headache and pain · 2026Review
- Calcitonin gene-related peptide differentially modulates intracellular calcium levels in response to depolarizing stimuli in trigeminal ganglion neurons and glial cells.Neuroscience · 2025Article
- Method for cryopreservation of brainstem pons and medulla oblongata tissue from Sprague Dawley rats for establishing primary mixed neuron-glia cell cultures.Brain research · 2025Article
- Unraveling the relationship between inflammation and cluster headache.Frontiers in neurology · 2025Review
- The effect of ponicidin on CFA-induced chronic inflammatory pain and its mechanism based on network pharmacology and molecular docking.Frontiers in medicine · 2025Article
- Article
- Neuroimmune interactions in the development and chronification of migraine headache.Trends in neurosciences · 2024Review
- The Brain, the Eating Plate, and the Gut Microbiome: Partners in Migraine Pathogenesis.Nutrients · 2024Review
- Method for cryopreservation of trigeminal ganglion for establishing primary cultures of neurons and glia.Journal of neuroscience methods · 2024Article
- Inflammation, brain connectivity, and neuromodulation in post-traumatic headache.Brain, behavior, & immunity - health · 2024Review
- Association of dietary vitamin C consumption with severe headache or migraine among adults: a cross-sectional study of NHANES 1999-2004.Frontiers in nutrition · 2024Article
- Calcitonin Gene-Related Peptide-Mediated Trigeminal Ganglionitis: The Biomolecular Link between Temporomandibular Disorders and Chronic Headaches.International journal of molecular sciences · 2023Review
- Article
- Biomarkers of Migraine: An Integrated Evaluation of Preclinical and Clinical Findings.International journal of molecular sciences · 2023Review
- Review
- 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 role of glutamate in orofacial pain.Frontiers in neuroscience · 2022Review
- The Role of Neuro-Immune Interactions in Chronic Pain: Implications for Clinical Practice.Journal of pain research · 2022Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Clinical and basic science data support an integral role of calcitonin gene-related peptide (CGRP) in migraine pathology. Following trigeminal nerve activation, afferent release of CGRP causes vasodilation while efferent release leads to pain. Although CGRP can also be secreted from cell bodies of trigeminal neurons located within the ganglion, the function of CGRP released in the ganglion is poorly understood. Initially, we showed that SNAP-25, a protein required for CGRP release, was localized in cell bodies of trigeminal ganglia neurons. We also found that satellite glial cells in the ganglia express the CGRP1 receptor protein RAMP1. To determine whether CGRP could directly activate glial cells, primary cultures of rat trigeminal ganglia were utilized to study the effects of CGRP on glial nitric oxide (NO) synthesis and release. Under our culture conditions, >95% of the cells expressed glial fibrillary acidic protein and RAMP1. While weak iNOS staining was observed in glia under basal conditions, CGRP treatment greatly increased glial iNOS expression and NO release. This stimulatory effect was blocked by the CGRP1 receptor antagonist, CGRP(8-37) peptide. Treatment of glial cultures with forskolin or cAMP also increased iNOS expression and stimulated NO release to levels similar to CGRP. To our knowledge, this is the first evidence that activation of CGRP1 receptors regulates glial iNOS and NO release. We propose that following trigeminal nerve activation, CGRP secretion from neuronal cell bodies activates satellite glial cells that release NO and initiate inflammatory events in the ganglia that contribute to peripheral sensitization in migraine.
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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.