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Immunohistochemical characterization of calcitonin gene-related peptide in the trigeminal system of the familial hemiplegic migraine 1 knock-in mouse.
Cephalalgia 2011; 31(13):1368-80C

Abstract

INTRODUCTION

Familial hemiplegic migraine type 1 (FHM-1) is caused by mutations in the CACNA1A gene, with the R192Q mutation being the most common. Elevated calcitonin gene-related peptide (CGRP) levels in acute migraine and clinical trials using CGRP receptor antagonists suggest CGRP-related mechanisms are important in migraine.

METHODS

Wild-type and R192Q knock-in mice were anaesthetized and perfused. Using immunohistochemical staining, the expression of CGRP in the trigeminocervical complex (TCC) and in the trigeminal and dorsal root ganglia was characterized.

RESULTS

There was a 38% reduction in the percentage of CGRP-immunoreactive cells in the trigeminal ganglia (p < 0.001) of R192Q knock-in mice compared to wild-type animals. The size distribution profile of CGRP-immunoreactive cells within the trigeminal ganglia demonstrated no significant difference in cell diameter between the two groups (p ≥ 0.56). CGRP expression was also reduced in thoracic ganglia of R192Q knock-in mice (21% vs. 27% in wild-type group; p < 0.05), but not in other ganglia. In addition, decreased CGRP immunoreactivity was observed in the superficial laminae of the TCC in R192Q knock-in mice, when compared to the control group (p < 0.005).

CONCLUSION

The data demonstrates that the FHM-1 CACNA1A mutation alters CGRP expression in the trigeminal ganglion and TCC. This suggests further study of these animals is warranted to characterize better the role of these mutations in the neurobiology of migraine.

Authors+Show Affiliations

University of California San Francisco, San Francisco, 1701 Divisadero St, San Francisco, CA 94115, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

21893556

Citation

Mathew, Rammya, et al. "Immunohistochemical Characterization of Calcitonin Gene-related Peptide in the Trigeminal System of the Familial Hemiplegic Migraine 1 Knock-in Mouse." Cephalalgia : an International Journal of Headache, vol. 31, no. 13, 2011, pp. 1368-80.
Mathew R, Andreou AP, Chami L, et al. Immunohistochemical characterization of calcitonin gene-related peptide in the trigeminal system of the familial hemiplegic migraine 1 knock-in mouse. Cephalalgia. 2011;31(13):1368-80.
Mathew, R., Andreou, A. P., Chami, L., Bergerot, A., van den Maagdenberg, A. M., Ferrari, M. D., & Goadsby, P. J. (2011). Immunohistochemical characterization of calcitonin gene-related peptide in the trigeminal system of the familial hemiplegic migraine 1 knock-in mouse. Cephalalgia : an International Journal of Headache, 31(13), pp. 1368-80. doi:10.1177/0333102411418847.
Mathew R, et al. Immunohistochemical Characterization of Calcitonin Gene-related Peptide in the Trigeminal System of the Familial Hemiplegic Migraine 1 Knock-in Mouse. Cephalalgia. 2011;31(13):1368-80. PubMed PMID: 21893556.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Immunohistochemical characterization of calcitonin gene-related peptide in the trigeminal system of the familial hemiplegic migraine 1 knock-in mouse. AU - Mathew,Rammya, AU - Andreou,Anna P, AU - Chami,Linda, AU - Bergerot,Astrid, AU - van den Maagdenberg,Arn Mjm, AU - Ferrari,Michel D, AU - Goadsby,Peter J, Y1 - 2011/09/05/ PY - 2011/9/7/entrez PY - 2011/9/7/pubmed PY - 2012/2/2/medline SP - 1368 EP - 80 JF - Cephalalgia : an international journal of headache JO - Cephalalgia VL - 31 IS - 13 N2 - INTRODUCTION: Familial hemiplegic migraine type 1 (FHM-1) is caused by mutations in the CACNA1A gene, with the R192Q mutation being the most common. Elevated calcitonin gene-related peptide (CGRP) levels in acute migraine and clinical trials using CGRP receptor antagonists suggest CGRP-related mechanisms are important in migraine. METHODS: Wild-type and R192Q knock-in mice were anaesthetized and perfused. Using immunohistochemical staining, the expression of CGRP in the trigeminocervical complex (TCC) and in the trigeminal and dorsal root ganglia was characterized. RESULTS: There was a 38% reduction in the percentage of CGRP-immunoreactive cells in the trigeminal ganglia (p < 0.001) of R192Q knock-in mice compared to wild-type animals. The size distribution profile of CGRP-immunoreactive cells within the trigeminal ganglia demonstrated no significant difference in cell diameter between the two groups (p ≥ 0.56). CGRP expression was also reduced in thoracic ganglia of R192Q knock-in mice (21% vs. 27% in wild-type group; p < 0.05), but not in other ganglia. In addition, decreased CGRP immunoreactivity was observed in the superficial laminae of the TCC in R192Q knock-in mice, when compared to the control group (p < 0.005). CONCLUSION: The data demonstrates that the FHM-1 CACNA1A mutation alters CGRP expression in the trigeminal ganglion and TCC. This suggests further study of these animals is warranted to characterize better the role of these mutations in the neurobiology of migraine. SN - 1468-2982 UR - https://www.unboundmedicine.com/medline/citation/21893556/Immunohistochemical_characterization_of_calcitonin_gene_related_peptide_in_the_trigeminal_system_of_the_familial_hemiplegic_migraine_1_knock_in_mouse_ L2 - http://journals.sagepub.com/doi/full/10.1177/0333102411418847?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -