UNIT 9.1 Dural Inflammation Model of Migraine Pain

  1. Lee A. Phebus,
  2. Kirk W. Johnson

Published Online: 1 MAY 2001

DOI: 10.1002/0471142301.ns0901s06

Current Protocols in Neuroscience

Current Protocols in Neuroscience

How to Cite

Phebus, L. A. and Johnson, K. W. 2001. Dural Inflammation Model of Migraine Pain. Current Protocols in Neuroscience. 6:9.1:9.1.1–9.1.9.

Author Information

  1. Eli Lilly and Company, Indianapolis, Indiana

Publication History

  1. Published Online: 1 MAY 2001
  2. Published Print: FEB 1999


The cause of migraine pain is controversial. One recently proposed theory is that migraine pain may originate from inflammation of the meninges, particularly the dural membranes that surround the brain. This theory proposes that, during a migraine, there is an idiopathic activation of trigeminal sensory afferents, resulting in nociceptive transmission to the CNS as well as the release of pro-inflammatory substances in the periphery, particularly the dura. Dural inflammation is thought to lower the nociceptive threshold of dural afferents and facilitate nociceptive transmission to the central nervous system. In the procedure described in this unit, trigeminal sensory afferents are activated by electrically stimulating the trigeminal ganglion. This stimulation causes trigeminal peripheral sensory afferents to depolarize, inflammatory substances to be released from these afferents, and dural inflammation to appear. Dural inflammation is quantified by measuring plasma protein extravasation. The basic protocol describes this model in rats, and the alternate protocol describes the analogous procedure in guinea pigs.