The kinase Mammalian Target of Rapamycin (mTOR) plays a pivotal role in cellular metabolism and growth across diverse cell types. In neurons, mTOR assumes critical importance for both neuronal development and plasticity. Dysregulation of mTOR has been implicated in mTORopathies, including Tuberous Sclerosis Complex (TSC) and associated brain disorders like epilepsy. Despite its predominant cytoplasmic localization, several studies have reported the presence of mTOR in the nucleus. Through mass spectrometry analysis, we identified Brg1, the catalytic subunit of the BAF chromatin remodelling complex, as one of the nuclear interactors of mTOR. Consequently, our study aimed to delve into the mTOR-Brg1 interaction within the nucleus and its implications for neuronal development and disease. Using in vitro cultured rat neurons, our data confirmed an increased nuclear mTOR-Brg1 interaction following kainic acid (KA) treatment, highlighting mTOR-induced phosphorylation of Brg1. Additionally, we observed that modulation of mTOR and the proteasome influenced the nuclear presence of Brg1, suggesting proteasome -mediated degradation of Brg1 in the nucleus upon KA treatment. Consistent with these findings, the downregulation of Brg1 expression was noted upon TSC2 loss, resulting in mTOR hyperactivation in neurons. Ca2+ imaging and morphometric analysis unveiled striking similarities between neurons with silenced TSC2 and those lacking Brg1. Collectively, our findings indicate that neuronal activity induces alterations in the function of the Brg1-containing BAF complex through mTOR. The research was financed under the NCN MAESTRO grant 2020/38/A/NZ3/00447.