IndraLab

Statements

SCN1A activates sodium(1+). 9 / 9
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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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"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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"Mutations in SCN1A cause the sodium channel to have a short recovery time from fast inactivation."
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"SCN1A mediates the voltage-dependent sodium ion permeability of excitable membranes (primarily the inhibitory GABA-ergic interneurons) of the central nervous system via the α1 subunit of the neuronal voltage-gated sodium channel Nav1.1 [72]."
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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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"SCN1A encodes the α1 subunit of the neuronal voltage-gated sodium (Nav1.1), which mediates the voltage-dependent sodium ion permeability of excitable membranes of the CNS."
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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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"Endogenous sodium currents are mainly mediated by Nav1.6 and Nav1.7, but also Nav1.1, Nav1.2, Nav1.3 and Nav1.9 at low levels ( Lee et al., 2019 )."
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