IndraLab

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Mutated SCN1A inhibits sodium(1+). 7 / 7
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"Mechanistically, Scn1a mutations reduce sodium currents primarly in GABAergic interneurons, which impairs their electrical excitability, creates an imbalance in the ratio of excitation and inhibition in neural circuits, and promotes general hyperexcitability and seizures (Colasante et al., 2020; Kalume et al., 2013; Liautard et al., 2013; Martin et al., 2010; Ogiwara et al., 2007; Yu et al., 2006)."
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"In addition, the model experiment of gene knockout mice for simulating human channel diseases has verified that SCN1A mutation causes reduced expression level of sodium channel subtype Nav1.1, leading to decreased excitatory of inhibitory neurons, functional decline in inhibitory loop and increased neuronal excitability, which are necessary for the onset of epileptic seizures [XREF_BIBR]."
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"All of these SCN1A mutations lead to severely attenuated inward sodium currents due to reduced expression of SCN1A RNA and protein in inhibitory GABAergic interneurons (Sugawara et al. 2003; Ohmori et al. 2006; Bechi et al. 2012)."
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"Differential effects on sodium current impairments by distinct SCN1A mutations in GABAergic neurons derived from Dravet syndrome patients."
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"These results suggest that this SCN1A mutation predominantly impairs sodium channel activity in interneurons, leading to decreased inhibition."
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"3 In mouse models of DS, the Scn1a mutation reduces sodium currents and excitability in inhibitory interneurons.4, 5, 6, 7 As a result, this causes an imbalance between inhibition and excitation, leading to general hyperexcitability."
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"SCN1A mutations have been proposed to preferentially impair the sodium channel activity of GABAergic interneurons, diminishing their activity [XREF_BIBR]."
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