Altered neuronal excitability in neurodevelopmental disorders can have profound implications for adult brain function. Understanding the critical time windows determining the clinical outcomes and lasting changes induced during these periods is therefore crucial. In our mouse model of developmental and epileptic encephalopathy (DEE) harboring a patient-derived Scn2a (p.A263V) mutation that results in a gain-of-function of Nav1.2 channels, Scn2a mutants exhibit a transient increase in excitability of hippocampal pyramidal neurons in vitro during the neonatal period. In vivo, homozygous Scn2a mutants start having seizures as early as postnatal day three, and both homozygous and heterozygous mutants have frequent seizures in the subsequent two weeks of development. To assess the resulting adult seizure profile and interictal activity, we conducted ECoG telemetry recordings from the somatosensory cortex. We found that seizures persisted only in homozygous Scn2a mutants. In addition, theta oscillation power and frequency for homozygous and gamma oscillation power for both homozygous and heterozygous mutants were altered. To determine the long-term consequences of neonatal hippocampal seizures for network function, we performed multichannel hippocampal depth profile local field potential recordings. Homozygous mutants displayed reduced mid-gamma frequency across all hippocampal layers and changes in the modulation index between theta phases and gamma oscillation amplitudes. These findings suggest neonatal hyperexcitability induces lasting changes, with gene-dose-dependent alterations indicative of increased cortical excitability exclusive to p.A263V homozygotes. Future work will involve testing genetic tools, including antisense oligonucleotides and CRISPRi, to treat animals during specific vulnerable time windows, aiming to prevent seizures and normalize observed network differences.