SCN2A encodes the Nav1.2 voltage-gated sodium channel subunit, which is crucial for the initiation, propagation, and backpropagation of action potentials. During human and mouse brain development, Nav1.2 is the dominant axonal Nav isoform. Genetic SCN2A variants are associated with neurodevelopmental disorders such as epilepsy, ASD, ID, and schizophrenia. Nav1.2 gain-of-function variants have been shown to cause epilepsy and SUDEP, but the network changes driving epileptogenesis during development are not known. Given the dominant role of Nav1.2 during hippocampal development we hypothesize that characterizing cellular and network dysfunction associated with Nav1.2 gain-of-function during early postnatal development will be key to understanding epileptogenesis and associated behavioral comorbidities. We therefore engineered a patient-derived SCN2A mouse model based on the p.A263V GOF variant, which is associated with a broad clinical spectrum ranging from self-limiting neonatal/infantile seizures to intractable, neonatal-onset epileptic encephalopathy.To quantify the dynamics of hippocampal network activity and any pathological network changes, we conducted depth recordings from hippocampal and cortical regions in awake, head-fixed mouse pups. Hippocampal seizures were observed in heterozygous and homozygous pups hippocampal seizures as early as postnatal day (PN)2-3. The quantification of depth profiles and dynamics of early Sharp Waves (eSPWs) in the hippocampal CA1 region revealed alterations in the distribution and amplitude of eSPWs that originated from the CA3 region. Furthermore, seizure epochs were often preceded by a synchronized burst of neuronal activity originating from CA3. Together, our data suggest a dominant role of SCN2A GOF-induced increased CA3 excitability in driving early epileptogenesis in mouse hippocampus.