Data from: Scn2a insufficiency alters spontaneous neuronal Ca2+ activity in somatosensory cortex during wakefulness

<p class="MsoNormal">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<em> <span>i</span>n vitro </em>studies showed PTV reduce action potential firing, consequences at <em>in vivo</em> 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 <span>Ca²⁺</span> imaging and electrocorticography (ECoG) in awake mice showed that spontaneous <span>Ca²⁺</span> transients in somatosensory cortical neurons, as well as their pairwise co-activities were generally decreased in Scn2a ASO mice during spontaneous awake state and induced seizure state. The reduction of neuronal activities and paired co-activity are mechanisms associated with motor, social and cognitive deficits observed in our mouse model of severe Scn2a insufficiency, indicating these are likely mechanisms driving SCN2A PTV pathology.</p>