scholarly journals Insights into migraine mechanisms and CaV2.1 calcium channel function from mouse models of familial hemiplegic migraine

2010 ◽  
Vol 588 (11) ◽  
pp. 1871-1878 ◽  
Author(s):  
Daniela Pietrobon
Keyword(s):  
Calcium Channel ◽  
Mouse Models ◽  
Familial Hemiplegic Migraine ◽  
Hemiplegic Migraine ◽  
Channel Function

scholarly journals CaV2.1 P/Q-type calcium channel alternative splicing affects the functional impact of familial hemiplegic migraine mutations: Implications for calcium channelopathies

Channels ◽  
2009 ◽  
Vol 3 (2) ◽  
pp. 110-121 ◽  
Author(s):  
Paul J. Adams ◽  
Esperanza Garcia ◽  
Laurence S. David ◽  
Kirk J. Mulatz ◽  
Sian D. Spacey ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Calcium Channel ◽  
Familial Hemiplegic Migraine ◽  
Hemiplegic Migraine ◽  
Functional Impact

Mouse models to study L-type calcium channel function

2005 ◽  
Vol 106 (3) ◽  
pp. 347-355 ◽  
Author(s):  
Sven Moosmang ◽  
Peter Lenhardt ◽  
Nicole Haider ◽  
Franz Hofmann ◽  
Jörg W. Wegener
Keyword(s):  
Calcium Channel ◽  
Mouse Models ◽  
Channel Function

scholarly journals Mouse Models of Familial Hemiplegic Migraine for Studying Migraine Pathophysiology

2019 ◽  
Vol 17 (10) ◽  
pp. 961-973 ◽  
Author(s):  
Anisa Dehghani ◽  
Hulya Karatas
Keyword(s):  
Mouse Models ◽  
Mutant Mouse ◽  
Single Gene ◽  
Gene Mutations ◽  
Familial Hemiplegic Migraine ◽  
Mutant Mice ◽  
Hemiplegic Migraine ◽  
Migraine Pathophysiology ◽  
Behavioral Mechanisms ◽  
Shed Light

Migraine, an extremely disabling neurological disorder, has a strong genetic component. Since monogenic migraines (resulting from mutations or changes in a single gene) may help researchers discover migraine pathophysiology, transgenic mice models harboring gene mutations identified in Familial Hemiplegic Migraine (FHM) patients have been generated. Studies in these FHM mutant mice models have shed light on the mechanisms of migraine and may aid in the identification of novel targets for treatment. More specifically, the studies shed light on how gene mutations, hormones, and other factors impact the pathophysiology of migraine. The models may also be of relevance to researchers outside the field of migraine as some of their aspects are relevant to pain in general. Additionally, because of the comorbidities associated with migraine, they share similarities with the mutant mouse models of epilepsy, stroke, and perhaps depression. Here, we review the experimental data obtained from these mutant mice and focus on how they can be used to investigate the pathophysiology of migraine, including synaptic plasticity, neuroinflammation, metabolite alterations, and molecular and behavioral mechanisms of pain.

The Clinical Spectrum of Familial Hemiplegic Migraine Associated with Mutations in a Neuronal Calcium Channel

2001 ◽  
Vol 345 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Anne Ducros ◽  
Christian Denier ◽  
Anne Joutel ◽  
Michaëlle Cecillon ◽  
Christelle Lescoat ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Familial Hemiplegic Migraine ◽  
Clinical Spectrum ◽  
Hemiplegic Migraine ◽  
Neuronal Calcium Channel

scholarly journals Gating Deficiency in a Familial Hemiplegic Migraine Type 1 Mutant P/Q-type Calcium Channel

2005 ◽  
Vol 280 (25) ◽  
pp. 24064-24071 ◽  
Author(s):  
Curtis F. Barrett ◽  
Yu-Qing Cao ◽  
Richard W. Tsien
Keyword(s):  
Calcium Channel ◽  
Familial Hemiplegic Migraine ◽  
Hemiplegic Migraine

Variable clinical expression of mutations in the P/Q-type calcium channel gene in familial hemiplegic migraine

Neurology ◽  
1998 ◽  
Vol 50 (4) ◽  
pp. 1105-1111 ◽  
Author(s):  
G. M. Terwindt ◽  
R. A. Ophoff ◽  
J. Haan ◽  
M. N. Vergouwe ◽  
R. van Eijk ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Familial Hemiplegic Migraine ◽  
Clinical Expression ◽  
Hemiplegic Migraine ◽  
Channel Gene
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