Mice that express a fluorescent synaptic receptor reveal the interactions between neurons in unprecedented detail.

These short reports from Spectrum journalists highlight some of the autism-related findings that caught our attention at the meeting this past week.

Activating certain receptors in the amygdala — a treatment that runs counter to a leading theory of what causes the condition — can reverse some traits in rats.

Even partial loss of the gene impairs the mouse brain’s ability to respond to sensory experiences, which may explain why people with SYNGAP1 mutations tend to have learning difficulties and a high pain tolerance.

Jolting a bundle of nerve fibers deep in the brain restores learning and memory in mice with mutations of the autism-linked gene CDKL5.

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.

Spectrum spoke with three Black scientists about why they got into autism research, what keeps them excited about their work and how the field could become more diverse.

A new atlas lays bare how synapses, or the junctions between neurons, change from birth to old age in mice.

The mood-stabilizing drug lithium seems to ease repetitive behaviors seen in mice missing SHANK3, an autism gene.