Mice missing DLG2, a protein central to neuronal activity, are anxious, sleep poorly and overgroom themselves.

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.

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.

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.

Families of children with mutations in a gene called SYNGAP1 have spurred research into the effects of the mutations on people — and how to treat them.

A new technique leads to neuron cultures of consistent quality, enabling scientists to study how autism mutations alter neurons.

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.

The brains of rats exposed in utero to the seizure drug valproate show a significant increase in brain size around the time of birth.