IndraLab

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SCN1A activates sodium(1+). 6 / 6
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"Scn1a can enhance persistent inward sodium currents, and recent studies indicate that a mutation in this gene might play a role in migraine development and in epilepsy [179,180]."
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"In particular, we use a small molecule to show that selective NaV1.1 inhibition (a) decreases sodium currents in colon-innervating dorsal root ganglion neurons, (b) reduces colonic nociceptor mechanical responses, and (c) normalizes the enhanced visceromotor response to distension observed in 2 mouse models of irritable bowel syndrome."
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"Three recognized sodium channel gene EEs are caused by mutations in SCN8A, SCN1A (Dravet syndrome), SCN2A, and SCN8A."
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"Dravet syndrome (DS) is a childhood epilepsy syndrome caused by heterozygous mutations in the SCN1A gene encoding voltage gated sodium channel Na v 1.1."
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"The mismatch was first noted when hemizygous reduction of the Scn1a subunit was found to dramatically reduce sodium current in mouse interneurons, while sparing pyramidal neurons, despite apparently equivalent levels of gene expression."
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"SCN1A loss-of-function impairs sodium currents and spiking in hippocampal GABAergic interneurons, without a detectable effect on excitatory pyramidal neurons."
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