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Significance Many autism risk genes, such asSyngap1 , regulate synapse plasticity, and disruptions to this subcellular process are thought to underlie behavioral deficits. However, behavior emerges through experience-driven dynamics within neural ensembles or groups of coactivated neurons. It is currently unclear how genetic regulation of synapse plasticity contributes to experience-dependent changes to cortical ensemble activity. Our data demonstrate that disruptions to synapse-level strengthening mechanisms inSyngap1 mice underlies impairments to balanced plasticity within cortical ensembles driven by novel sensory experience. Because not all neurons in ensembles were sensitive toSyngap1 regulation, we propose that additional genetic mechanisms are also initiated in response to experience to effectively redistribute activity within cortical networks.

Syngap1 regulates experience-dependent cortical ensemble plasticity by promoting in vivo excitatory synapse strengthening