NMDA receptors (NMDARs) are tetrameric complexes composed of two GluN1 subunits and two regulatory subunits. In the hippocampus, the more expressed regulatory subunits are GluN2A and GluN2B. These subunits are encoded by grin genes, whose expression is tightly regulated. In humans, mutations in grin2A are associated with complex phenotypes and reduced GluN2A expression. In our laboratory, we previously demonstrated that GluN2A knockdown (GluN2A-KD) induces a more immature neuronal phenotype, accompanied by decreased GluN1 protein levels. Interestingly, dendritic GluN1 clusters remained unaffected in GluN2A-KD neurons. Moreover, we observed a shift in GluN1 splicing variants, favoring isoforms associated with enhanced forward trafficking. Given that grin1 splicing variants undergo dynamic changes during embryonic development and exhibit distinct distribution in brain structures, we aimed to investigate variant postnatal developmental dynamics and compare this distribution with that observed in GluN2A-KD neurons. To this end, we extracted hippocampal mRNA at different postnatal stages and analyzed the distribution of grin1 variants, comparing it to the pattern observed in our GluN2A-KD model. Our results suggest developmental changes in grin1 splicing variant expression and suggest that GluN2A-KD alters this pattern, contributing to the observed immature neuronal phenotype.