SynGAP regulates synaptic plasticity and cognition independently of its catalytic activity.

SynGAP is an abundant synaptic GTPase-activating protein (GAP) critical for synaptic plasticity, learning, memory, and cognition. Mutations in in humans result in intellectual disability, autistic-like behaviors, and epilepsy. Heterozygous -knockout mice display deficits in synaptic plasticity, learning, and memory and exhibit seizures.

Mouse models of -related intellectual disability.

SYNGAP1 is a Ras-GTPase-activating protein highly enriched at excitatory synapses in the brain. De novo loss-of-function mutations in are a major cause of genetically defined neurodevelopmental disorders (NDDs). These mutations are highly penetrant and cause -related intellectual disability (SRID), an NDD characterized by cognitive impairment, social deficits, early-onset seizures, and sleep disturbances.

Mouse models of -related intellectual disability.

Unlabelled: SYNGAP1 is a Ras-GTPase activating protein highly enriched at excitatory synapses in the brain. loss-of-function mutations in are a major cause of genetically defined neurodevelopmental disorders (NDD). These mutations are highly penetrant and cause -related intellectual disability (SRID), a NDD characterized by cognitive impairment, social deficits, early-onset seizures, and sleep disturbances (1-5).

Experience-Dependent and Differential Regulation of Local and Long-Range Excitatory Neocortical Circuits by Postsynaptic Mef2c.

Development of proper cortical circuits requires an interaction of sensory experience and genetic programs. Little is known of how experience and specific transcription factors interact to determine the development of specific neocortical circuits. Here, we demonstrate that the activity-dependent transcription factor, Myocyte enhancer factor-2C (Mef2c), differentially regulates development of local versus long-range excitatory synaptic inputs onto layer 2/3 neurons in the somatosensory neocortex in vivo.