Journal
ANNALS OF NEUROLOGY
Volume 69, Issue 5, Pages 855-865Publisher
WILEY
DOI: 10.1002/ana.22329
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Funding
- NIH National Institutes of Neurological Disorders and Stroke [NS069847, NS035611]
- Allergan
- Endo
- GlaxoSmithKline
- Merck
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Objective: Cortical spreading depression (CSD) has long been implicated in migraine attacks that begin with visual aura. Having shown that a wave of CSD can trigger long-lasting activation of meningeal nociceptors-the first-order neurons of the trigeminovascular pathway thought to underlie migraine headache-we now report that CSD can activate central trigeminovascular neurons in the spinal trigeminal nucleus (C1-2). Methods: Stimulation of the cortex with pinprick or KCl granule was used to induce CSD in anesthetized rats. Neuronal activity was monitored in C1-2 using single-unit recording. Results: In 25 trigeminovascular neurons activated by CSD, mean firing rate (spikes/s) increased from 3.6 +/- 1.2 before CSD (baseline) to 6.1 +/- 1.8 after CSD (p < 0.0001) for a period >13 minutes. Neuronal activity returned to baseline level after 30.0 +/- 3.1 minutes in 14 units, and remained elevated for 66.0 +/- 8.3 (22-108) minutes through the entire recording period in the other 11 units. Neuronal activation began within 0.9 +/- 0.4 (0-2.5) minutes after CSD in 7 neurons located in laminae I-II, or after a latency of 25.1 +/- 4.0 (7-75) minutes in 9 neurons located in laminae I-II, and 9 neurons located in laminae III-V. In 27 trigeminovascular neurons not activated by CSD, mean firing rate was 2.0 +/- 0.7 at baseline and 1.8 +/- 0.7 after CSD. Interpretation: We propose that CSD constitutes a nociceptive stimulus capable of activating peripheral and central trigeminovascular neurons that underlie the headache of migraine with aura. ANN NEUROL 2011; 69: 855-865
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