| First Author | Uchino K | Year | 2023 |
| Journal | Biochem Biophys Res Commun | Volume | 643 |
| Pages | 169-174 | PubMed ID | 36610382 |
| Mgi Jnum | J:333501 | Mgi Id | MGI:7430489 |
| Doi | 10.1016/j.bbrc.2022.12.084 | Citation | Uchino K, et al. (2023) Astrocyte Ca(2+) signaling is facilitated in Scn1a(+/-) mouse model of Dravet syndrome. Biochem Biophys Res Commun 643:169-174 |
| abstractText | 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 Ca(2+) signaling in astrocytes using genetically modified mice that have a loss-of-function mutation in Scn1a. We found that the slope of spontaneous Ca(2+) spiking was increased without a change in amplitude in Scn1a(+/-) astrocytes. In addition, ATP-induced transient Ca(2+) influx and the slope of Ca(2+) spiking were also increased in Scn1a(+/-) astrocytes. These data indicate that perturbed Ca(2+) dynamics in astrocytes may be involved in the pathogenesis of DS. |
