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 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.  

Neurons from mice that model fragile X syndrome may fire signals more readily than neurons from controls, according to a study published 5 October in The Journal of Neuroscience. The results suggest a cause for the high incidence of seizures in individuals with the syndrome.

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.

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gene MeCP2 show a gradual decline in vision, and too much inhibitory signaling in the visual cortex, according to unpublished research presented Thursday in Washington, D.C.

An autism-linked protein helps wire neurons together, according to two studies published in late September.

Mice lacking a copy of SHANK3, a gene associated with autism and intellectual disability, show marked improvements in brain signaling after being treated with insulin-like growth factor 1, according to unpublished findings presented Saturday at the International Congress of Human Genetics in Montreal, Canada.

Researchers have engineered four new mouse lines that each show activation of a different subset of neurons in response to a blue light.

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.

A compound that shows promise as a treatment for fragile X syndrome alleviates repetitive behaviors in mice, but unexpectedly makes them less social.