The SWI/SNF (BAF) complex regulates gene transcription through chromatin remodeling, with SMARCA2 (BRM) serving as a core ATP hydrolysis enzyme subunit in this complex. Clinical cases have revealed that mutations in SMARCA2 (BRM) lead to Nicolaides-Baraitser syndrome, causing symptoms such as cortical dysplasia, corpus callosum agenesis, intellectual disability, and epilepsy. However, the pathogenic mechanisms of SMARCA2 (BRM) in neurodevelopment remain unclear. In this study, we hypothesize SMARCA2(BRM) mutation impairs the neural development through altering the chromatin remodeling of the SWI/SNF(BAF) complex and affecting the downstream gene expression. To explore the role of SMARCA2 (BRM) in neurodevelopment. In utero electroporation is used to inhibit SMARCA2 (BRM) or overexpress mutant SMARCA2 (BRM) in the brains of mouse embryos to investigate its impact on neurodevelopment. Cell transfection and immunofluorescence staining are employed to observe the protein expression, subcellular distribution, and neuronal differentiation of SMARCA2 (BRM). Through the experiments mentioned above, we found that knockdown of SMARCA2 (BRM) in neurons led to migration delay at E18.5. No significant differences in protein expression are observed between wild-type and mutant SMARCA2 (BRM) in N2A cell transfection. In cellular localization, SMARCA2 (BRM) is mainly expressed in the nucleus, but cells transfected with mutant SMARCA2 (BRM) show predominant cytoplasmic localization. This study identifies a potential role for SMARCA2 (BRM) in neurodevelopment and chromatin remodeling and proposes possible pathological mechanisms of SMARCA2 (BRM) mutations.