Expression of artemin and GFR[alpha]3 in an animal model of migraine: possible role in the pathogenesis of this disorder

Background Neurotrophic factors have been implicated in hyperalgesia and peripheral levels of these molecules are altered in migraine pathophysiology. Artemin, a vasculature-derived neurotrophic factor, contributes to pain modulation and trigeminal primary afferent sensitization through binding its...

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Bibliographic Details
Published in:Journal of headache and pain 2016-09, Vol.17, p.1
Main Authors: Shang, Hai-qiong, Wang, Yan, Mao, Yan-yan, Kong, Li-gang, Sun, Gao-ying, Xu, Lei, Zhang, Dao-gong, Han, Yue-chen, Li, Jian-feng, Wang, Hai-bo, Fan, Zhao-min
Format: Article
Language:English
Subjects:
Brain-derived neurotrophic factor
Headaches
Migraine
Pathogenesis
Smooth muscle
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Summary:Background Neurotrophic factors have been implicated in hyperalgesia and peripheral levels of these molecules are altered in migraine pathophysiology. Artemin, a vasculature-derived neurotrophic factor, contributes to pain modulation and trigeminal primary afferent sensitization through binding its selective receptor GFR[alpha]3. The distribution of artemin and GFR[alpha]3 in the dura mater raises an anatomy supports that they may be involved in migraine. In this study we evaluated the expression of artemin and GFR[alpha]3 in an animal migraine model that may be relevant for migraine. Methods In this study, using a rat migraine model by administration of nitroglycerin (NTG), we investigated the expression of artemin in the dura mater and GFR[alpha]3 in the trigeminal ganglia (TG) by means of quantitative reverse transcription-polymerase chain reaction, western blot and immunofluorescence labeling. Results Artemin immunoreactivity was found in the smooth muscle cells of dural vasculature and GFR[alpha]3 was present in cytoplasm of TG neurons. The mRNA levels of artemin and GFR[alpha]3 were significantly elevated after NTG treatment at 2 and 4 h respectively (P
ISSN:1129-2369
1129-2377
DOI:10.1186/s10194-016-0673-2