scholarly journals Upregulation of IL-1 Receptor Antagonist in a Mouse Model of Migraine

2019 ◽  
Vol 9 (7) ◽  
pp. 172 ◽  
Author(s):  
Salvo Lombardo ◽  
Emanuela Mazzon ◽  
Maria Basile ◽  
Eugenio Cavalli ◽  
Placido Bramanti ◽  
...  
Keyword(s):  
Mouse Model ◽  
Receptor Antagonist ◽  
Spreading Depression ◽  
Occipital Cortex ◽  
Familial Hemiplegic Migraine ◽  
Therapeutic Strategies ◽  
Hemiplegic Migraine ◽  
Inflammatory Genes ◽  
Glial Depolarization

Migraine is a disorder characterized by attacks of monolateral headaches, often accompanied by nausea, vomiting, and photophobia. Around 30% of patients also report aura symptoms. The cause of the aura is believed to be related to the cortical spreading depression (CSD), a wave of neuronal and glial depolarization originating in the occipital cortex, followed by temporary neuronal silencing. During a migraine attack, increased expression of inflammatory mediators, along with a decrease in the expression of anti-inflammatory genes, have been observed. The aim of this study was to evaluate the expression of inflammatory genes, in particular that of IL-1 receptor antagonist (IL-1RN), following CSD in a mouse model of familial hemiplegic migraine type 1 (FHM-1). We show here that the expression of IL-1RN was upregulated after the CSD, suggesting a possible attempt to modulate the inflammatory response. This study allows researchers to better understand the development of the disease and aids in the search for new therapeutic strategies in migraine.

scholarly journals Enhanced Subcortical Spreading Depression in Familial Hemiplegic Migraine Type 1 Mutant Mice

2011 ◽  
Vol 31 (15) ◽  
pp. 5755-5763 ◽  
Author(s):  
K. Eikermann-Haerter ◽  
I. Yuzawa ◽  
T. Qin ◽  
Y. Wang ◽  
K. Baek ◽  
...  
Keyword(s):  
Spreading Depression ◽  
Familial Hemiplegic Migraine ◽  
Mutant Mice ◽  
Hemiplegic Migraine

Stress hormone corticosterone enhances susceptibility to cortical spreading depression in familial hemiplegic migraine type 1 mutant mice

2015 ◽  
Vol 263 ◽  
pp. 214-220 ◽  
Author(s):  
Reinald Shyti ◽  
Katharina Eikermann-Haerter ◽  
Sandra H. van Heiningen ◽  
Onno C. Meijer ◽  
Cenk Ayata ◽  
...  
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Familial Hemiplegic Migraine ◽  
Mutant Mice ◽  
Stress Hormone ◽  
Hemiplegic Migraine

scholarly journals Androgenic suppression of spreading depression in familial hemiplegic migraine type 1 mutant mice

2009 ◽  
Vol 66 (4) ◽  
pp. 564-568 ◽  
Author(s):  
Katharina Eikermann-Haerter ◽  
Michael J. Baum ◽  
Michel D. Ferrari ◽  
Arn M.J.M. van den Maagdenberg ◽  
Michael A. Moskowitz ◽  
...  
Keyword(s):  
Spreading Depression ◽  
Familial Hemiplegic Migraine ◽  
Mutant Mice ◽  
Hemiplegic Migraine

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

Cephalalgia ◽  
2020 ◽  
Vol 40 (11) ◽  
pp. 1177-1190
Author(s):  
Chunhua Tang ◽  
Miyuki Unekawa ◽  
Mamoru Shibata ◽  
Yutaka Tomita ◽  
Yoshikane Izawa ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mice ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Orthologous Gene ◽  
Underlying Mechanism ◽  
Familial Hemiplegic Migraine ◽  
Wild Type ◽  
Hemiplegic Migraine ◽  
Fos Expression

Background Cortical spreading depression is thought to be the underlying mechanism of migraine aura. In 2006, three relatives having the point mutation E700K in ATP1A2 exon 15 were diagnosed with familial hemiplegic migraine 2 characterized by complicated forms of aura. Here, we generated a transgenic mouse model having the human E700K mutation in the Atp1a2 orthologous gene. Objective To investigate the characteristics of cortical spreading depression in a mouse model with E700K mutation in the Atp1a2. 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 ( p < 0.01) and longer full-width-at-half-maximum ( p < 0.01) than wild-type animals, representing a slower recovery from direct current potential deflection. The cortical spreading depression threshold tended to be lower in Tg, especially in females. c-Fos-positive cells were significantly enhanced in the ipsilateral somatosensory cortex, piriform cortex, amygdala and striatum (each p < 0.05 vs. contralateral side). Numbers of c-Fos positive cells were significantly higher in the ipsilateral amygdala of Tg, as compared with wild-type animals ( p < 0.01). 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.

scholarly journals Migraine: Calcium Channels and Glia

2021 ◽  
Vol 22 (5) ◽  
pp. 2688
Author(s):  
Marta Kowalska ◽  
Michał Prendecki ◽  
Thomas Piekut ◽  
Wojciech Kozubski ◽  
Jolanta Dorszewska
Keyword(s):  
Migraine With Aura ◽  
Migraine Without Aura ◽  
Spreading Depression ◽  
Adult Population ◽  
Familial Hemiplegic Migraine ◽  
Trigeminovascular System ◽  
Hemiplegic Migraine ◽  
Monogenic Form ◽  
Calcitonin Gene

Migraine is a common neurological disease that affects about 11% of the adult population. The disease is divided into two main clinical subtypes: migraine with aura and migraine without aura. According to the neurovascular theory of migraine, the activation of the trigeminovascular system (TGVS) and the release of numerous neuropeptides, including calcitonin gene-related peptide (CGRP) are involved in headache pathogenesis. TGVS can be activated by cortical spreading depression (CSD), a phenomenon responsible for the aura. The mechanism of CSD, stemming in part from aberrant interactions between neurons and glia have been studied in models of familial hemiplegic migraine (FHM), a rare monogenic form of migraine with aura. The present review focuses on those interactions, especially as seen in FHM type 1, a variant of the disease caused by a mutation in CACNA1A, which encodes the α1A subunit of the P/Q-type voltage-gated calcium channel.

Sign in / Sign up

Export Citation Format

Share Document