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.

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.

Mice missing the Rett syndrome gene MeCP2 show a gradual decline in vision, and too much inhibitory signaling in the visual cortex, according to unpublished research presented Thursday in Washington, D.C.

The Rett syndrome gene MeCP2 may subtly regulate the expression of genes across the genome by altering DNA structure.