A large scientific research company debuted seven new rat models of autism Tuesday evening in Washington, D.C. Two of the models, one lacking FMR1 and the other lacking NLGN3, show some unexpected new characteristics.

In a video interview at the 2011 Society for Neuroscience annual meeting in Washington, D.C., Caroline Blanchard describes some of the unusual behaviors that suggest that the BTBR mouse is a good model for autism.

Researchers have engineered 20 mouse lines that allow them to manipulate genes in specific neuronal circuits. The resource, reported 22 September in Neuron, will allow researchers to better explore the role of interneurons, which dampen signals in the brain, in mouse models of autism. 

Drugs that act on the adrenaline system can alleviate autism-like symptoms in a rat model of the disorder, according to unpublished research presented Sunday in Washington, D.C.

Mice with a mutation in the Rett syndrome gene are more social than controls, according to a study published 11 September in Behavioral Genetics. The results, based on detailed observation of social behavior, support previous studies showing that Rett syndrome mouse models do not have severe social deficits.

In a video interview at the 2011 Society for Neuroscience annual meeting in Washington, D.C., Joseph Buxbaum discussed the importance of mice with mutations in SHANK3, a leading autism candidate gene.

A protein involved in the cascade of interactions at the junctions between neurons points to a potential therapy for fragile X syndrome, according to unpublished data presented at the 2011 Society for Neuroscience annual meeting in Washington, D.C.

Mice that have an excess of the Rett syndrome protein MeCP2 have biochemical and neuronal characteristics that are strikingly similar to those of mice that completely lack the protein, according to unpublished research described Sunday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.

Mice lacking the autism risk gene SHANK2 show social deficits and are extremely hyperactive, according to unpublished research presented Saturday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.

Deleting the Rett syndrome gene in a subset of neurons, instead of throughout the body, dramatically lowers the number of genes that are dysregulated in those neurons, according to results presented in a poster session Saturday at the 2011 Society for Neuroscience annual meeting in Washington, D.C.