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Published on: June 2, 2014
Mast cell degranulation activates a pain pathway underlying migraine headache
Dan Levy1, Rami Burstein, Vanessa Kainz
1Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Harvard Institutes of Medicine, Room 856, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. dlevy1@bidmc.harvard.edu
Pain
|April 27, 2007
Summary
Dural mast cell degranulation activates meningeal nociceptors, contributing to intracranial headaches like migraine. This neuroimmune interaction highlights a key mechanism in trigeminal pain pathway activation.
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- Intracranial headaches, including migraine, are linked to prolonged meningeal nociceptor activation.
- The precise mechanisms driving this nociceptor activation remain largely unknown.
Purpose of the Study:
- To investigate the hypothesis that dural mast cells can locally activate meningeal nociceptors via neuroimmune interactions.
- To explore the role of mast cell degranulation in trigeminal pain pathway activation.
Main Methods:
- In vivo electrophysiological single unit recording of rat meningeal nociceptors.
- Induction of mast cell degranulation using compound 48/80.
- Assessment of phosphorylated extracellular signal-regulated kinase (pERK) and c-fos expression as markers of activation.
Main Results:
- Degranulation of dural mast cells led to prolonged excitation of meningeal nociceptors.
- Increased pERK expression indicated nociceptor activation.
- Downstream activation of the spinal trigeminal nucleus was evidenced by increased c-fos expression.
Conclusions:
- Dural mast cell degranulation is directly linked to the prolonged activation of meningeal nociceptors.
- This neuroimmune mechanism contributes to the trigeminal pain pathway activation underlying intracranial headaches such as migraine.
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