Scn2a insufficiency alters spontaneous neuronal Ca²⁺ activity in somatosensory cortex during wakefulness.

ABSTRACT: SCN2A protein-truncating variants (PTV) can result in neurological disorders such as autism spectrum disorder and intellectual disability, but they are less likely to cause epilepsy in comparison to missense variants. While in vitro studies showed PTV reduce action potential firing, consequences at in vivo network level remain elusive. Here, we generated a mouse model of Scn2a insufficiency using antisense oligonucleotides (Scn2a ASO mice), which recapitulated key clinical feature of SCN2A PTV disorders. Simultaneous two-photon Ca²⁺ imaging and electrocorticography (ECoG) in awake mice showed that spontaneous Ca²⁺ transients in somatosensory cortical neurons, as well as their pairwise co-activities were generally decreased in Scn2a ASO mice during sponta

SUBMITTER: Li M 

PROVIDER: S-EPMC10590963 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature