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Astrocyte Ca2+ signaling is facilitated in Scn1a+/− mouse model of Dravet syndrome.
- Source :
-
Biochemical & Biophysical Research Communications . Feb2023, Vol. 643, p169-174. 6p. - Publication Year :
- 2023
-
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, Nav 1.1 , 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. • Ca2+ spiking was significantly faster in astrocytes cultured from Scn1a+/− mice. • ATP-induced Ca2+ spiking was also significant in astrocytes cultured from Scn1a+/− mice. • Restoring Ca2+ signaling in astrocytes would lead to the development of novel therapies for epilepsy. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 0006291X
- Volume :
- 643
- Database :
- Academic Search Index
- Journal :
- Biochemical & Biophysical Research Communications
- Publication Type :
- Academic Journal
- Accession number :
- 161361115
- Full Text :
- https://doi.org/10.1016/j.bbrc.2022.12.084