A drug that helps promote gene expression reduces repetitive behaviors and improves memory and sociability in a mouse model of autism.

The first animal model of MYT1L syndrome suggests that fast-maturing neurons lead to the unusually small brains, social deficits and other traits seen in people with the condition.

Mice exposed to unusually low levels of the placental hormone allopregnanolone in the womb show atypical brain development and autism-like behaviors.

Altered electrical activity in the neurons of mice with a mutated copy of SCN2A may explain the animals’ autism-like social behaviors.

Mounting evidence suggests that autism often involves upsets in homeostatic plasticity, a set of processes neurons use to stabilize their activity. These disruptions result from a range of autism-linked mutations and may help to explain the condition’s famed heterogeneity.

The finding that MDMA and an experimental serotonin agonist increase sociability across six different model mice suggests that disparate autism-linked mutations converge on the same underlying pathways.

Deleterious mutations in an autism-associated gene can make neurons hyperexcitable, raising the risk of epileptic seizures.

Neurons in mice with an autism-linked mutation sprout extraneous protrusions, an overgrowth accompanied by above-average motor learning. Inhibiting a cell signaling pathway reverses the effect.

A mutation in the autism-linked gene SHANK3 changes how neurons encode information about social agency in mice.

A mouse model hints that genes linked to inflammation in some women may increase the likelihood of autism in their children.