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EHMTI-0093. Investigation of 5-HT2B receptor pathways with relevance to a mouse migraine model

  • M Kremser
  • A Hunfeld
  • H Lübbert
Open Access
Meeting abstract
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Keywords

Migraine Dura Mater Chronic Migraine mCPP Neurogenic Inflammation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Introduction

Recent research raises the question whether the serotonin 2B receptor (5-HT2B) plays a role in the pathogenesis of migraine. Clinical studies revealed that the 5-HT2B/2C agonist meta-Chlorophenylpiperazine (mCPP) induces migraine-like headache more likely in migraineurs than in subjects without a history of migraine. We therefore developed an animal model for chronic migraine, where we are able to induce a neurogenic inflammation in the dura mater of hypoxic mice with 5-HT2B agonists. This inflammation can be blocked by specific 5-HT2B inhibitors.

Until now little is known about the 5-HT2B receptor: It is expressed on endothelial cells of blood vessels, but it may also be present on other cell types. Like most of the other serotonin receptors it is a G protein-coupled receptor, but the native signal transduction pathway after receptor activation is not clear yet.

Aims

Investigation of the 5-HT2B receptor in a primary cell culture system to determine native signal transduction pathways.

Methods

Cultivation of primary cells. Validation of the presence of the receptor. Signal transduction assays.

Results

Stimulation with the 5-HT2B/2C agonist mCPP induced concentration-dependent ERK phosphorylation in 5-HT2B positive primary cells.

Conclusions

Activation of the 5-HT2B receptors may stimulate cell proliferation and angiogenesis and therefore alter the vascular system of the dura mater, which may result in a higher susceptibility for migraine.

No conflict of interest.

Copyright information

© Kremser et al; licensee Springer. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Authors and Affiliations

  • M Kremser
    • 1
  • A Hunfeld
    • 1
  • H Lübbert
    • 1
  1. 1.Department of Animal PhysiologyFaculty of Biology and BiotechnologyBochumGermany

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