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.

The protein missing in people with fragile X syndrome regulates the activity of more than 800 other proteins, including some key players in autism, according to a study published 22 July in Cell. Many of these autism-associated proteins cluster on either side of the synapse, the junction between neurons.

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.

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.

A new mouse model of 15q duplication syndrome, a genetic disorder associated with autism, falls short of recapitulating the symptoms of the syndrome. But it nonetheless points to a cluster of well-known risk genes as the most likely culprits.

Spontaneous and inherited mutations in SHANK3 both inhibit the protein’s role at synapses, the junctions between neurons, according to a study published 24 May in Molecular Psychiatry.

A new online database that compiles genomic sequence information for 162 mouse strains shows that classical laboratory strains have limited genetic diversity, according to a report published 29 May in Nature Genetics.

Mice with a mutation in SHANK3, a leading autism candidate gene, show moderate social defects, including less-than-normal interest in other mice. The findings, published 27 May in Cell, suggest that mutations in different sites on the gene can lead to different behaviors. This paper was retracted on 17 January 2013. Associate director of research Alan Packer discusses the implications of the retraction here.

MeCP2, the protein that’s missing or mutated in Rett syndrome, is crucial for remodeling neural circuits in response to vision, according to a study published in April in Neuron.

Mice lacking CNTNAP2, a gene linked to autism and language impairment, show behaviors and brain abnormalities that reflect those seen in people with disorder, according to new findings presented Thursday at the International Meeting for Autism Research in San Diego.