Abstract | BACKGROUND: Acute cutaneous neurogenic inflammation initiated by activation of transient receptor potential vanilloid-1 (TRPV1) receptors following intradermal injection of capsaicin is mediated mainly by dorsal root reflexes (DRRs). Inflammatory neuropeptides are suggested to be released from primary afferent nociceptors participating in inflammation. However, no direct evidence demonstrates that the release of inflammatory substances is due to the triggering of DRRs and how activation of TRPV1 receptors initiates neurogenic inflammation via triggering DRRs. RESULTS: CONCLUSION: Our data suggest that 1) the generation of DRRs is critical for driving the release of neuropeptides antidromically from primary afferent nociceptors; 2) activation of TRPV1 receptors in primary afferent nociceptors following intradermal capsaicin injection initiates this process; 3) the released CGRP and SP participate in neurogenic inflammation.
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Authors | Qing Lin, Dingge Li, Xijin Xu, Xiaoju Zou, Li Fang |
Journal | Molecular pain
(Mol Pain)
Vol. 3
Pg. 30
(Oct 25 2007)
ISSN: 1744-8069 [Electronic] United States |
PMID | 17961222
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Analgesics
- GABA Antagonists
- Peptide Fragments
- Receptors, Neurokinin-1
- TRPV Cation Channels
- Trpv1 protein, rat
- calcitonin gene-related peptide (8-37)
- Substance P
- spantide
- Calcitonin Gene-Related Peptide
- capsazepine
- Capsaicin
- Bicuculline
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Topics |
- Analgesics
(pharmacology)
- Animals
- Bicuculline
(pharmacology)
- Calcitonin Gene-Related Peptide
(metabolism, pharmacology, toxicity)
- Capsaicin
(administration & dosage, analogs & derivatives, toxicity)
- Edema
(chemically induced, etiology)
- GABA Antagonists
(pharmacology)
- Injections, Intradermal
- Neurogenic Inflammation
(chemically induced, etiology)
- Peptide Fragments
(pharmacology)
- Rats
- Receptors, Neurokinin-1
(agonists, physiology)
- Reflex
- Spinal Nerve Roots
(drug effects, physiopathology)
- Substance P
(analogs & derivatives, metabolism, pharmacology, toxicity)
- TRPV Cation Channels
(agonists, physiology)
- Vasodilation
(drug effects)
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