Regulation of calcitonin gene-related peptide release from rat trigeminal nucleus caudalis slices in vitro

David W. Jenkins, Christopher J. Langmead, Andrew A. Parsons, Paul J. Strijbos

Research output: Contribution to journalArticleResearchpeer-review

54 Citations (Scopus)

Abstract

Calcitonin gene-related peptide (CGRP) released from trigeminal primary afferents has been implicated in the pathophysiology of migraine. Here, we have used an in vitro slice preparation to investigate its release from nerve terminals in the rat trigeminal nucleus caudalis. Extracellular-calcium dependent CGRP release was stimulated by both capsaicin and neuronal depolarization with KCl. The capsaicin (1 μM)-evoked CGRP release was blocked by capsazepine and was also attenuated in the presence of the cyclooxygenase inhibitor, indomethacin, an effect that was reversed when slices were stimulated with capsaicin in the presence of the cyclooxygenase metabolite, prostaglandin E 2. Taken together, these data further highlight the importance of prostaglandins as enhancers of neuropeptide release and suggest that CGRP released from the central terminals of trigeminal neurones has the potential to be involved in the transmission of nociceptive information of relevance to migraine headache.

Original languageEnglish
Pages (from-to)241-244
Number of pages4
JournalNeuroscience Letters
Volume366
Issue number3
DOIs
Publication statusPublished - 19 Aug 2004
Externally publishedYes

Keywords

  • Calcitonin gene-related peptide
  • Migraine
  • Prostaglandin E
  • Superfusion
  • Trigeminal nucleus caudalis

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