Vikaas Sohal and his colleagues set out to test the hypothesis that excessive entry of calcium into neurons within the medial prefrontal cortex (mPFC) impairs social behavior and contributes to additional aspects of autism. The researchers learned that the excessive entry of calcium does not affect all neurons in the mPFC equally. Rather, neurons in the mPFC can be divided into different subpopulations, and the excessive entry of calcium has a profound effect on one of these subpopulations.

Large-scale population studies are valuable for elucidating gene-environment interactions that contribute to the risk of autism. Young Shin Kim and her colleagues at Yale University are assembling a large-scale collection of autism-related data from a group of children in South Korea who show a variety of symptoms across the autism spectrum.

Many children with autism have unusually high numbers of synapses, or connections between neurons, particularly in the cortex, which may result from overgrowth and a disruption of neuronal pruning during childhood. Pruning and reshaping of neurons pares down the number of synapses in the brain while eliminating inappropriate synapses that lead to over-connectivity between brain regions, and possibly inappropriate learning, behavior and seizures. David Sulzer and his colleagues at Columbia University hypothesize that autism-associated mutations in the tuberous sclerosis gene, TSC, can cause over-connectivity when the target of TSC, the mTOR pathway, interferes with normal neuronal pruning.