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A Cacna1a knockin migraine mouse model with increased susceptibility to cortical spreading depression.

Neuron | Mar 4, 2004

http://www.ncbi.nlm.nih.gov/pubmed/15003170

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.

Pubmed ID: 15003170 RIS Download

Mesh terms: Animals | Calcium Channels | Calcium Channels, N-Type | Calcium Channels, P-Type | Calcium Channels, Q-Type | Cells, Cultured | Cortical Spreading Depression | Disease Models, Animal | Female | Genetic Predisposition to Disease | Humans | Male | Mice | Mice, Mutant Strains | Mice, Transgenic | Migraine with Aura | Motor Endplate | Mutation | Recombination, Genetic

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Associated grants

  • Agency: Telethon, Id: E.0847
  • Agency: Telethon, Id: E.1297

Mouse Genome Informatics (Data, Gene Annotation)

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