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

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 dep...

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Bibliographic Details
Published in:Neuroscience letters 2004-08, Vol.366 (3), p.241-244
Main Authors: Jenkins, David W, Langmead, Christopher J, Parsons, Andrew A, Strijbos, Paul J
Format: Article
Language:English
Subjects:
Analysis of Variance
Animals
Biological and medical sciences
Calcitonin gene-related peptide
Calcitonin Gene-Related Peptide - metabolism
Calcium - metabolism
Capsaicin - analogs & derivatives
Capsaicin - pharmacology
Cyclooxygenase Inhibitors - pharmacology
Dinoprostone - pharmacology
Drug Interactions
Enzyme-Linked Immunosorbent Assay - methods
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation
In Vitro Techniques
Indomethacin - pharmacology
Male
Medical sciences
Migraine
Neurology
Potassium Chloride - pharmacology
Prostaglandin E 2
Rats
Rats, Sprague-Dawley
Superfusion
Trigeminal Caudal Nucleus - metabolism
Trigeminal nucleus caudalis
Vascular diseases and vascular malformations of the nervous system
Vertebrates: nervous system and sense organs
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Summary: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.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2004.05.067