Mice with an extra copy of MeCP2, the Rett syndrome gene, have impaired signaling between neurons in the hippocampus, a brain region that plays an important role in memory, according to a study published 29 February in The Journal of Neuroscience.

Mutations in more than 100 autism-associated genes lead to shared neurobiological deficits in mice, including alterations in the shape of their brains and changes to the electrical properties of neurons, according to a study published 20 February in Molecular Autism.

Neurobeachin, or NBEA, an autism–associated gene, may regulate the transport of signaling molecules to neuronal branches, according to a study published 22 November in Nature Communications.

A compound that boosts inhibitory signals in the brain could treat hyperactivity and excitability in mice that model fragile X syndrome, according to a study published 8 November in Developmental Neuroscience.

A new technique efficiently screens for compounds that enhance or inhibit the formation of synapses, the junctions between neurons, according to a study published 25 October in Nature Communications.

The brain abnormalities characteristic of tuberous sclerosis may begin early in development and involve malfunctioning of neuronal precursors, according to studies of two different mouse models of the disorder published in October.

The etiology of autism may be best understood as an impairment of neuronal circuits, specifically interneurons that dampen signals in the brain, says neuroscientist Gordon Fishell.  

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. 

Neurexins, autism-linked proteins that organize synapses, the junctions between neurons, function in only a subset of cells in the brain, according to data presented in a poster Monday 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.