NMDARs play a crucial role in synaptic plasticity under physiological and pathological conditions. NMDARs are composed of two GluN1 subunits and two regulatory subunits. Among the regulatory subunits, GluN2A and GluN2B are the most abundantly expressed in brain regions associated with cognition, such as the hippocampus. GluN2B is predominantly found in immature structures, while GluN2A is characteristic of mature ones. This balance between GluN2 subunit types is essential for proper glutamatergic neurotransmission, and its disruption is implicated in various pathological conditions. Alterations in GluN2A expression, often due to GRIN2A mutations, have been linked to complex phenotypes that contribute to neurodevelopmental disorders, including the onset of seizures. However, the role of reduced GluN2A expression in these phenotypes remains poorly understood. We assessed neuronal functionality and morphology in GluN2A knock-down neurons and found enhanced responses to glutamate stimulation and increased dendritic spine density. However, while total NMDAR levels were reduced, surface GluN2A levels remained comparable to controls. These findings suggest that new spines are immature, as well as neurons too. Furthermore, we observed that GluN2A reduction altered AMPAR subunit expression and localization. Taken together, these findings help to explain the delayed maturation observed in GluN2A-KD neurons, which may underline the increased susceptibility to seizures observed in vivo.