IndraLab

Statements


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"Lower levels of SCN1A, SCN2A, SCN3A, SCN4A and SCN8A expression have also been reported in heart and shown to contribute approximately 23% of the total functional sodium channels in mouse ventricular myocytes and 27% in human atrial myocytes, based on TTX sensitivity."

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"Consequently, Scn1a loss of function selectively reduces sodium current density in inhibitory interneurons (Yu et al., 2006), and behavioral deficits in an Scn1a haploinsufficiency mouse model of Dravet syndrome can be rescued by augmenting GABAergic activity with clonazepam (Han et al., 2012)."

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"Dysfunction of Nav1.1 decreases sodium currents in different types of GABAergic interneurons, especially the parvalbumin (PV)-positive interneurons where Nav1.1 is predominantly expressed [11, 12]."

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"It is caused by loss-of-function mutations in the gene SCN1A encoding brain sodium channel Nav1.1, which specifically impair action potential firing by GABAergic inhibitory interneurons and disinhibit neural circuits in the brain."