Journal
PAIN
Volume 130, Issue 1-2, Pages 166-176Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.pain.2007.03.012
Keywords
meningeal nociceptors; dura; mast cells; migraine headache
Categories
Funding
- NIDCR NIH HHS [R01 DE013347-05, R01 DE013347] Funding Source: Medline
- NINDS NIH HHS [R01NS032534, R01 NS032534, R01NS046502, R01 NS046502-04, R01 NS046502] Funding Source: Medline
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Intracranial headaches such as that of migraine are generally accepted to be mediated by prolonged activation of meningeal nociceptors but the mechanisms responsible for such nociceptor activation are poorly understood. In this study, we examined the hypothesis that meningeal nociceptors can be activated locally through a neuroimmune interaction with resident mast cells, granulated immune cells that densely populate the dura mater. Using in vivo electrophysiological single unit recording of meningeal nociceptors in the rat we observed that degranulation of dural mast cells using intraperitoneal administration of the basic secretagogue agent compound 48/80 (2 mg/kg) induced a prolonged state of excitation in meningeal nociceptors. Such activation was accompanied by increased expression of the phosphorylated form of the extracellular signal-regulated kinase (pERK), an anatomical marker for nociceptor activation. Mast cell-induced nociceptor interaction was also associated with downstream activation of the spinal trigeminal nucleus as indicated by an increase in c-fos expression. Our findings provide evidence linking dural mast cell degranulation to prolonged activation of the trigeminal pain pathway believed to underlie intracranial headaches such as that of migraine. (C) 2007 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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