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• W4313480211 abstract "Dravet syndrome (DS) is an infantile-onset epileptic encephalopathy. More than 80% of DS patients have a heterozygous mutation in SCN1A, which encodes a subunit of the voltage-gated sodium channel, Nav1.1, in neurons. The roles played by astrocytes, the most abundant glial cell type in the brain, have been investigated in the pathogenesis of epilepsy; however, the specific involvement of astrocytes in DS has not been clarified. In this study, we evaluated Ca2+ signaling in astrocytes using genetically modified mice that have a loss-of-function mutation in Scn1a. We found that the slope of spontaneous Ca2+ spiking was increased without a change in amplitude in Scn1a+/- astrocytes. In addition, ATP-induced transient Ca2+ influx and the slope of Ca2+ spiking were also increased in Scn1a+/- astrocytes. These data indicate that perturbed Ca2+ dynamics in astrocytes may be involved in the pathogenesis of DS." @default.
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• W4313480211 date "2023-02-01" @default.
• W4313480211 modified "2023-09-27" @default.
• W4313480211 title "Astrocyte Ca2+ signaling is facilitated in Scn1a+/− mouse model of Dravet syndrome" @default.
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• W4313480211 doi "https://doi.org/10.1016/j.bbrc.2022.12.084" @default.
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