Mice missing an autism gene called SHANK3 tend to be hypersensitive to touch, which may stem from underactivity of neurons that normally dampen sensory responses.

Neurons in mice that lack an autism gene called CNTNAP2 do not differentiate well between social and nonsocial smells — an issue that seems to stem from haphazard neuronal firing.

Researchers have analyzed thousands of brain organoids derived from six autistic people, gaining the potential to rapidly screen drugs.

Studies of Rett syndrome hint at genes, cells and brain circuits that may be involved in autism — and may pave the way to treatments for both conditions.

Deleting an autism gene called TRIO derails neurons’ journey to their destination.

Injecting cells called interneurons into the brains of a mouse model of autism restores typical social behavior. But the reason for this effect is a puzzle.

Mice missing a copy of CHD8, a top autism gene, show a signaling imbalance in their brains — a finding in line with a popular hypothesis about autism’s origins.

An experimental drug that muffles the activity of neurons in the skin moderates heightened reactions to touch in six mouse models of autism.

The signaling imbalance theory holds that the brains of autistic people are hyper-excitable because of either excess neuronal activity or weak brakes on that activity.

An analysis of four mouse models negates certain assumptions underlying the signaling imbalance theory of autism.