Abstract
with the function of SynGAP to repress Ras, soluble fractions of SYNGAP+/-neurons, showed higher Ras-GTP levels, and consequently, an hyperactivation of the MAPK/ERK signaling pathway.In future experiments we aim to recapitulate AMPAR trafficking defects by assessing surface AMPAR expression in SYNGAP+/-neurons.The morphological and biochemical changes observed, along with the functional impact of SYNGAP1 haploinsufficiency in our human cell model, may provide a promising path for further exploration into the molecular mechanisms underlying SYNGAP1 disease.This could potentially open the way for the development of novel therapeutic strategies for this disorder.