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Publication year - 2004
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1111/j.1526-4610.2004.04164_8.x
Subject(s) - nociceptin receptor , cluster headache , trigeminal ganglion , calcitonin gene related peptide , medicine , endocrinology , neuropeptide , substance p , opioid peptide , receptor , opioid , anesthesia , migraine , biology , neuroscience , sensory system
The trigeminal innervation of the dura and its vessels has a prominent role in the mechanism of cluster headache. Nociceptin, an opioid neuropeptide, is the endogenous ligand of the OP‐4 receptor, with both algesic and analgesic properties depending on the site of action. Nociceptin and its receptor are expressed by trigeminal ganglion cells where they colocalize with calcitonin gene‐related peptide (CGRP), a marker peptide of the trigeminovascular neurones. Nociceptin inhibits neurogenic dural vasodilatation, a phenomenon related to trigeminovascular activation. To explore its possible involvement in cluster headache, we studied circulating levels of nociceptin when attack‐free during the cluster period, and also after the termination of the cluster period, using radioimmunoassay. In 14 cluster headache patients nociceptin levels during the cluster period were significantly lower than in age‐, and sex‐matched controls (4.91 ± 1.96 vs. 9.58 ± 2.57 pg/ml; P < .01). After the termination of the cluster period nociceptin levels (8.60 ± 1.47 pg/ml) were not statistically different from controls. Nociceptin levels did not correlate with age, length of disease, or episode length. Lower nociceptin levels during the cluster period may result in a defective regulation of trigeminal activity that might not protect sufficiently against the attacks.