Haploinsufficiency of SYNGAP1 (synaptic RAS GTPase activating protein 1) in humans can lead to intellectual disability and epilepsy, and Syngap1+/− mice exhibit impaired cognition. Here, in mice, heterozygous knockout of Syngap1 in developing forebrain pyramidal neurons, but not in GABAergic neurons, was sufficient to replicate the Syngap1+/− mouse phenotype. Reduction of SYNGAP1 levels in adult mice had no effect on cognition or pyramidal neuron excitability, indicating that the cognitive impairment in Syngap1+/− mice is due to altered development of forebrain excitatory neurons.