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Christensen SL, Rasmussen RH, Ernstsen C, et al. CGRP-dependent signalling pathways involved in mouse models of GTN- cilostazol- and levcromakalim-induced migraine. Cephalalgia. 2021;41(14):1413-1426doi: 10.1177/03331024211038884.
Christensen, S. L., Rasmussen, R. H., Ernstsen, C., La Cour, S., David, A., Chaker, J., Haanes, K. A., Christensen, S. T., Olesen, J., & Kristensen, D. M. (2021). CGRP-dependent signalling pathways involved in mouse models of GTN- cilostazol- and levcromakalim-induced migraine. Cephalalgia : an international journal of headache, 41(14), 1413-1426. https://doi.org/10.1177/03331024211038884
Christensen, Sarah L, et al. "CGRP-dependent signalling pathways involved in mouse models of GTN- cilostazol- and levcromakalim-induced migraine." Cephalalgia : an international journal of headache vol. 41,14 (2021): 1413-1426. doi: https://doi.org/10.1177/03331024211038884
Christensen SL, Rasmussen RH, Ernstsen C, La Cour S, David A, Chaker J, Haanes KA, Christensen ST, Olesen J, Kristensen DM. CGRP-dependent signalling pathways involved in mouse models of GTN- cilostazol- and levcromakalim-induced migraine. Cephalalgia. 2021 Dec;41(14):1413-1426. doi: 10.1177/03331024211038884. Epub 2021 Aug 18. PMID: 34407650.
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Cephalalgia. 2021 Dec;41(14):1413-1426. doi: 10.1177/03331024211038884. Epub 2021 Aug 18.

CGRP-dependent signalling pathways involved in mouse models of GTN- cilostazol- and levcromakalim-induced migraine.

Cephalalgia : an international journal of headache

Sarah L Christensen, Rikke H Rasmussen, Charlotte Ernstsen, Sanne La Cour, Arthur David, Jade Chaker, Kristian A Haanes, Søren T Christensen, Jes Olesen, David M Kristensen

Affiliations

  1. Danish Headache Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmark.
  2. Univ Rennes, Inserm, EHESP, Irset (Institut de recherche en santé, environnement et travail) - UMR_S 1085, Rennes, France.
  3. Department of Clinical Experimental Research, 70590Rigshospitalet Glostrup, Rigshospitalet Glostrup, Denmark.
  4. Department of Biology, Section of Cell Biology and Physiology, University of Copenhagen, Denmark.

PMID: 34407650 DOI: 10.1177/03331024211038884

Abstract

RESULTS: Glyceryl trinitrate-induced hypersensitivity was dependent on both prostaglandins and transient receptor potential cation channel, subfamily A, member 1, whereas cilostazol- and levcromakalim-induced hypersensitivity were independent of both. All three migraine triggers activated calcitonin gene-related peptide signalling, as both receptor antagonism and antibody neutralisation of calcitonin gene-related peptide were effective inhibitors of hypersensitivity in all three models. Stimulation of trigeminal ganglia and brain stem tissue samples with cilostazol and levcromakalim did not result in release of calcitonin gene-related peptide, and vasodilation following levcromakalim stimulation was independent of CGRP receptor antagonism.

CONCLUSION: The mouse models of glyceryl trinitrate-, cilostazol- and levcromakalim- induced migraine all involve calcitonin gene-related peptide signalling in a complex interplay between different cell/tissue types. These models are useful in the study of migraine mechanisms.

Keywords: Crosstalk; RAMP1; TRPA1; in vivo; migraine pain signalling

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