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

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

A transplant of inhibitory neurons during the second week of life prevents social difficulties and a brain signaling imbalance in mice missing a copy of FOXG1.

Mice missing the autism-linked gene SHANK3 use more neurons to engage in social behavior than control mice do, reflecting a more disorganized, less efficient brain signaling network.

Worms and zebrafish missing both copies of the gene CHD7 have disrupted cellular signaling, a dearth of inhibitory neurons and behavior changes — all of which are reversed by the stimulant drug ephedrine.

The investigational drug arbaclofen makes autistic people’s brains respond to a visual task more like non-autistic people’s brains do.

The investigational drug arbaclofen may right an imbalance between inhibitory and excitatory signaling in the animals’ brains.

Mice missing a copy of chromosomal region 16p11.2 are slow to learn motor tasks and have dysfunction in a brain circuit associated with stress and movement, according to a new study. Normalizing this circuit’s activity corrects the learning deficit.

Researchers have devised a way to use fluorescent sensors to detect many different signaling molecules in a cell at once.