Abstract:
:Migraine is a common, disabling, multifactorial, episodic neurovascular disorder of unknown etiology. Familial hemiplegic migraine type 1 (FHM-1) is a Mendelian subtype of migraine with aura that is caused by missense mutations in the CACNA1A gene that encodes the alpha(1) subunit of neuronal Ca(v)2.1 Ca(2+) channels. We generated a knockin mouse model carrying the human pure FHM-1 R192Q mutation and found multiple gain-of-function effects. These include increased Ca(v)2.1 current density in cerebellar neurons, enhanced neurotransmission at the neuromuscular junction, and, in the intact animal, a reduced threshold and increased velocity of cortical spreading depression (CSD; the likely mechanism for the migraine aura). Our data show that the increased susceptibility for CSD and aura in migraine may be due to cortical hyperexcitability. The R192Q FHM-1 mouse is a promising animal model to study migraine mechanisms and treatments.
journal_name
Neuronjournal_title
Neuronauthors
van den Maagdenberg AM,Pietrobon D,Pizzorusso T,Kaja S,Broos LA,Cesetti T,van de Ven RC,Tottene A,van der Kaa J,Plomp JJ,Frants RR,Ferrari MDdoi
10.1016/s0896-6273(04)00085-6subject
Has Abstractpub_date
2004-03-04 00:00:00pages
701-10issue
5eissn
0896-6273issn
1097-4199pii
S0896627304000856journal_volume
41pub_type
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