Journal article
Vascular actions of peripheral CGRP in migraine-like photophobia in mice
Cephalalgia, Vol.40(14), pp.33310242094917-1604
08/18/2020
DOI: 10.1177/0333102420949173
PMID: 32811179
Abstract
Background Calcitonin gene-related peptide is recognized as a key player in migraine, yet the mechanisms and sites of calcitonin gene-related peptide action remain unknown. The efficacy of calcitonin gene-related peptide-blocking antibodies as preventative migraine drugs supports a peripheral site of action, such as the trigeminovasculature. Given the apparent disconnect between the importance of vasodilatory peptides in migraine and the prevailing opinion that vasodilation is an epiphenomenon, the goal of this study was to test whether vasodilation plays a role in calcitonin gene-related peptide-induced light aversive behavior in mice. Methods Systemic mean arterial pressure and light aversive behavior were measured after intraperitoneal administration of calcitonin gene-related peptide and vasoactive intestinal peptide in wild-type CD1 mice. The functional significance of vasodilation was tested by co-administration of a vasoconstrictor (phenylephrine, endothelin-1, or caffeine) with calcitonin gene-related peptide to normalize blood pressure during the light aversion assay. Results Both calcitonin gene-related peptide and vasoactive intestinal peptide induced light aversion that was associated with their effect on mean arterial pressure. Notably, vasoactive intestinal peptide caused relatively transient vasodilation and light aversion. Calcitonin gene-related peptide-induced light aversion was still observed even with normalized blood pressure. However, two of the agents, endothelin-1 and caffeine, did reduce the magnitude of light aversion. Conclusion We propose that perivascular calcitonin gene-related peptide causes light-aversive behavior in mice by both vasomotor and non-vasomotor mechanisms.
Details
- Title: Subtitle
- Vascular actions of peripheral CGRP in migraine-like photophobia in mice
- Creators
- Bianca N Mason - Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA, Brain and Behavior Sciences, Center for Advanced Pain Studies, University of Texas at Dallas, Richardson, TX, USAAnne-Sophie Wattiez - Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA, Center for the Prevention and Treatment of Visual Loss, Veterans Administration Health Center, Iowa City, IA, USALouis K Balcziak - Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA, Neuroscience Program, University of Iowa, Iowa City, IA, USAAdisa Kuburas - Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USAWilliam J Kutschke - Division of Cardiovascular Medicine, Department of Internal Medicine and Francois M Abboud Cardiovascular Research Center, University of Iowa, Iowa City, IA, USAAndrew F Russo - Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA, Center for the Prevention and Treatment of Visual Loss, Veterans Administration Health Center, Iowa City, IA, USA, Department of Neurology, University of Iowa, Iowa City, IA, USA
- Resource Type
- Journal article
- Publication Details
- Cephalalgia, Vol.40(14), pp.33310242094917-1604
- DOI
- 10.1177/0333102420949173
- PMID
- 32811179
- NLM abbreviation
- Cephalalgia
- ISSN
- 0333-1024
- eISSN
- 1468-2982
- Grant note
- DOI: 10.13039/100000738, name: U.S. Department of Veterans Affairs, award: 1I0RX002101; DOI: 10.13039/100000009, name: Foundation for the National Institutes of Health, award: NS075599, NS098825
- Language
- English
- Date published
- 08/18/2020
- Academic Unit
- Neurology; Molecular Physiology and Biophysics; Iowa Neuroscience Institute; Craniofacial Anomalies Research Center; Internal Medicine
- Record Identifier
- 9984070521402771
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