Characteristics of cortical spreading depression and c-Fos expression in transgenic mice having a mutation associated with familial hemiplegic migraine 2.


Journal

Cephalalgia : an international journal of headache
ISSN: 1468-2982
Titre abrégé: Cephalalgia
Pays: England
ID NLM: 8200710

Informations de publication

Date de publication:
10 2020
Historique:
pubmed: 3 6 2020
medline: 26 10 2021
entrez: 3 6 2020
Statut: ppublish

Résumé

Cortical spreading depression is thought to be the underlying mechanism of migraine aura. In 2006, three relatives having the point mutation E700K in To investigate the characteristics of cortical spreading depression in a mouse model with E700K mutation in the Cortical spreading depression was induced by applying stepwise increases of KCl concentration or electrical stimulation intensity to C57BL/6J-Tg(Atp1a2*E700K)9151Kwk mice (Tg, both sexes) and corresponding wild-type animals. Under urethane anesthesia, the responsiveness and threshold to cortical spreading depression were examined and the distribution of c-Fos expression, a neuronal activity marker, was immunohistochemically determined. Overall, Tg mice showed significantly faster propagation velocity ( The effect of cortical spreading depression may be greater in E700K transgenic mice than that in wild-type animals, while the threshold for cortical spreading depression shows little change. Higher c-Fos expression in the amygdala may indicate alterations of the limbic system in Tg, suggesting an enhanced linkage between cortical spreading depression and amygdala connectivity in familial hemiplegic migraine 2 patients.

Sections du résumé

BACKGROUND
Cortical spreading depression is thought to be the underlying mechanism of migraine aura. In 2006, three relatives having the point mutation E700K in
OBJECTIVE
To investigate the characteristics of cortical spreading depression in a mouse model with E700K mutation in the
METHODS
Cortical spreading depression was induced by applying stepwise increases of KCl concentration or electrical stimulation intensity to C57BL/6J-Tg(Atp1a2*E700K)9151Kwk mice (Tg, both sexes) and corresponding wild-type animals. Under urethane anesthesia, the responsiveness and threshold to cortical spreading depression were examined and the distribution of c-Fos expression, a neuronal activity marker, was immunohistochemically determined.
RESULTS
Overall, Tg mice showed significantly faster propagation velocity (
CONCLUSION
The effect of cortical spreading depression may be greater in E700K transgenic mice than that in wild-type animals, while the threshold for cortical spreading depression shows little change. Higher c-Fos expression in the amygdala may indicate alterations of the limbic system in Tg, suggesting an enhanced linkage between cortical spreading depression and amygdala connectivity in familial hemiplegic migraine 2 patients.

Identifiants

pubmed: 32484063
doi: 10.1177/0333102420929028
doi:

Substances chimiques

Proto-Oncogene Proteins c-fos 0
ATP1A2 protein, human EC 3.6.1.-
Sodium-Potassium-Exchanging ATPase EC 7.2.2.13

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1177-1190

Auteurs

Chunhua Tang (C)

Department of Neurology, Keio University School of Medicine, Tokyo, Japan.
Department of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.

Miyuki Unekawa (M)

Department of Neurology, Keio University School of Medicine, Tokyo, Japan.

Mamoru Shibata (M)

Department of Neurology, Keio University School of Medicine, Tokyo, Japan.

Yutaka Tomita (Y)

Department of Neurology, Keio University School of Medicine, Tokyo, Japan.

Yoshikane Izawa (Y)

Department of Neurology, Keio University School of Medicine, Tokyo, Japan.

Hiroki Sugimoto (H)

Division of Biology, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.

Keiko Ikeda (K)

Division of Biology, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.
Division of Physiology, International University of Health and Welfare, Narita, Japan.

Kiyoshi Kawakami (K)

Division of Biology, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.

Norihiro Suzuki (N)

Department of Neurology, Shonan Keiiku Hospital, Fujisawa, Japan.

Jin Nakahara (J)

Department of Neurology, Keio University School of Medicine, Tokyo, Japan.

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Classifications MeSH