Neurons in a mouse model of fragile X syndrome make more connections during a critical period in development compared with controls, but are slower to respond to signals.

Probiotic bacteria alleviate stress in healthy mice and modify the expression of receptors for a chemical messenger that inhibits signaling in the brain.

Researchers have created the first mouse model of Timothy syndrome, a rare genetic disorder that causes heart defects and autism. The findings appeared 30 August in the Proceedings of the National Academy of Sciences.

A new review suggests that sleep problems in neurodevelopmental disorders don’t just reflect underlying weaknesses in neural circuitry; they actively intensify these deficits.

MeCP2, the protein missing in people with Rett syndrome, enhances learning and memory by binding to key genes and either activating or inhibiting their expression, according to a study published 17 July in Nature Neuroscience. Adding a phosphate to the protein in response to neuronal activity releases MeCP2 from these genes, the study found.

By zapping mouse brains with blue and yellow light beams, scientists have manipulated the animals’ social behaviors and bolstered a popular theory of what causes autism.

Giving GLYX-13, a drug that targets an autism-associated brain pathway, to rats bred to be less social increases how much they communicate while playing.

Mice lacking SHANK1, a member of a family of autism-associated proteins, communicate less with their mothers and potential mates than controls do, according to a study published 9 June in PLoS One.

FOXP2, a gene tied to autism and language disorders, is needed for proper wiring of the developing brain, according to a study published 7 July in PLoS Genetics.

A multi-site collaborative venture between the U.S., Canada and Europe has created nearly 17,000 mouse embryonic stem cell lines, each lacking one of the genes in the mouse genome.