ArticleHeadache2026
TRPM3 activation causes CGRP release in trigeminal neurons: Implications for migraine mechanisms.
Article in Headache, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
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Who cites it
6 citing papers in PubMed.
- A delayed endothelial-glial mechanism for CGRP-induced migraine.The journal of headache and pain · 2026Review
- Calcitonin Gene-Related Peptide (CGRP): Biology, Signaling, Pathophysiological Roles, and Therapeutic Applications.International journal of molecular sciences · 2026Review
- CGRP-targeted migraine treatment and early pathophysiology in experimental subarachnoid hemorrhage.The journal of headache and pain · 2026Article
- From bench to bedside: relevant animal models across the migraine attack phases.The journal of headache and pain · 2026Review
- Functional characterisation of dura mater αCGRP degradation fragments at vascular, immune, and CGRP receptor targets.The journal of headache and pain · 2026Article
- The therapeutic pipeline in migraine: What does the future hold?Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundThe transient receptor potential melastatin 3 (TRPM3) ion channel has been implicated in sensory modulation and pain transmission and may contribute to migraine pathophysiology through calcitonin gene-related peptide (CGRP) release in the trigeminovascular system. This study aimed to investigate TRPM3 activation and its role in CGRP release, vasodilatory responses, and migraine-relevant behaviors using preclinical models.
methodsMale and female Sprague-Dawley rats were used to evaluate CGRP release from trigeminal ganglia (TG) and dura mater following stimulation with the TRPM3 agonist CIM0216. CGRP levels were quantified using ELISA. Myograph studies assessed vasodilation in the middle cerebral artery (MCA) and middle meningeal artery. Immunohistochemistry was used to examine TRPM3 and CGRP localization in TG, dura mater, MCA, and human dura mater. Potential behavioral responses to subcutaneous CIM0216 administration were assessed via mechanical sensitivity tests. Calcium responses to CIM0216 were investigated on CGRP neurons in the TG of transgenic female mice.
resultsTRPM3 channel activation with CIM0216 triggered CGRP release from TG at 100 μM, with indications of enhanced release in female tissues. Immunohistochemistry confirmed colocalization of the TRPM3 channel and CGRP in TG neurons. Additionally, TRPM3 expression was detected in arterial structures, indicating potential involvement in vascular regulation. Although CIM0216 induced CGRP release ex vivo, subcutaneous CIM0216 administration was unable to induce allodynia-like symptoms in rats. Application of CIM0216 induced an increase of cytosolic calcium in trigeminal CGRP neurons.
conclusionsTRPM3 activation triggers CGRP release and vasodilatation. The findings that TRPM3 induced CGRP release support further investigation of TRPM3 as a therapeutic target for migraine.
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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.