ArticleThe journal of headache and pain2025
Substance P release from rat dura mater is inversely correlated with CGRP release- experiments using glycerol trinitrate and anti-CGRP antibodies.
Article in The journal of headache and pain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
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Who cites it
3 citing papers in PubMed.
- A delayed endothelial-glial mechanism for CGRP-induced migraine.The journal of headache and pain · 2026Review
- CGRP: the immune system's double agent - context-dependent roles in inflammation, resolution and cancer.Frontiers in immunology · 2026Review
- Endogenous treatments for migraine pain.The journal of headache and pain · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe neuropeptides calcitonin gene-related peptide (CGRP) and substance P are important mediators of neurogenic inflammation when they are released from activated primary nociceptive afferents. It is long evident that neuropeptides play an important role in migraine pathophysiology, but the significance of neurogenic inflammation is still debated.
methodsIn an approved hemisected rodent head preparation, we measured CGRP release from the cranial dura mater in parallel with substance P release using animals pre-treated with anti-CGRP antibodies or control solutions.
resultsApart from the known decrease in CGRP release following antibody treatment, we found a significant inverse correlation of basal and stimulated CGRP versus substance P release across all experiments. The results are discussed in connection with our previously published data.
conclusionsAn increase in CGRP release seems to inhibit substance P release in meningeal structures possibly decreasing substance P-dependent plasma extravasation, which argues against a significant role of neurogenic inflammation in migraine.
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Registered trials
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