The α1 isoform of synGAP restricts the binding of AMPA-receptors and other regulatory proteins to PSD-95, and thus regulates synaptic strength.

Severe neurodevelopmental disorder risk gene functions are retained into adulthood and they contribute to disease phenotypes, indicating that these patients may respond to treatments throughout life.

Deletion of one copy of the postsynaptic density protein synGAP in rodents causes an increase in the level of the AMPA receptor auxiliary protein TARP in PSDs only in females.

Detailed SYNGAP1 splice variant characterization uncovers distinct isoform functions and biochemical properties contributing to critical aspects of neurodevelopment, providing previously unknown isoform-level insight into SYNGAP1-related cognitive disorders.

A knockin mouse line was made to label endogenous AMPA receptors, enabling direct observation of synaptic plasticity in behaving animals with single-synapse resolution across the entire brain.

Alternatively spliced C-terminal protein sequences encoded by the Syngap1 gene exhibit unique biochemical and functional properties in vivo, which explain in part how individual isoforms can promote cognitive functions and seizure protection.