Na+ channelopathies and epilepsy: recent advances and new perspectives.
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Phenytoin inhibits the persistent sodium current in neocortical neurons by modifying its inactivation propertiesImpaired action potential initiation in GABAergic interneurons causes hyperexcitable networks in an epileptic mouse model carrying a human Na(V)1.1 mutationEvaluation of Presumably Disease Causing SCN1A Variants in a Cohort of Common Epilepsy Syndromes.Nonfunctional NaV1.1 familial hemiplegic migraine mutant transformed into gain of function by partial rescue of folding defectsDravet syndrome: insights from in vitro experimental models.Divergent effects of the T1174S SCN1A mutation associated with seizures and hemiplegic migraine.Pure haploinsufficiency for Dravet syndrome Na(V)1.1 (SCN1A) sodium channel truncating mutations.Hippocampal hyperexcitability and specific epileptiform activity in a mouse model of Dravet syndrome.
P2860
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P2860
Na+ channelopathies and epilepsy: recent advances and new perspectives.
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article científic
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article scientifique
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articol științific
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articolo scientifico
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artigo científico
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artigo científico
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artigo científico
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artikel ilmiah
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artikull shkencor
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artículo científico
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name
Na+ channelopathies and epilepsy: recent advances and new perspectives.
@en
Na+ channelopathies and epilepsy: recent advances and new perspectives.
@nl
type
label
Na+ channelopathies and epilepsy: recent advances and new perspectives.
@en
Na+ channelopathies and epilepsy: recent advances and new perspectives.
@nl
prefLabel
Na+ channelopathies and epilepsy: recent advances and new perspectives.
@en
Na+ channelopathies and epilepsy: recent advances and new perspectives.
@nl
P2860
P356
P1476
Na+ channelopathies and epilepsy: recent advances and new perspectives
@en
P2093
Carla Marini
P2860
P304
P356
10.1586/ECP.10.20
P407
P577
2010-05-01T00:00:00Z