Prenatal exposure of rats to the epilepsy drug valproic acid leads to behavioral and brain features that resemble autism, in males more than in females, according to a study published in the March issue of the Journal of Neurochemistry.

An imbalance in the excitatory and inhibitory signaling between neurons seems to play a critical role in autism. What can we do with that information?

In 2003, John Rubenstein and Michael Merzenich first described the theory, now popular in autism, that the disorder reflects an imbalance between excitation and inhibition in the brain. Takao K. Hensch and Parizad M. Bilimoria review the paper and its impact on the field.

Elevated levels of EIF4E, which plays a key role in protein synthesis, lead to autism-like behaviors and abnormal neuronal signaling in mice, according to a study published 17 January in Nature.

Transcranial magnetic stimulation may provide a noninvasive approach to studying how connections in the human brain change in response to new information, and how that process is altered in autism, says Lindsay Oberman.

Neurons in mice that model fragile X syndrome show immature, overexcitable firing patterns, particularly during sleep, according to unpublished research presented last week at the Salk Institute, Fondation IPSEN and Nature Symposium on Biological Complexity in La Jolla, California.

Memantine, a drug used to treat Alzheimer’s disease, can reverse autism-like features in mice lacking one copy of the MEF2C gene, according to a poster presented last week at the Salk Institute, Fondation IPSEN and Nature Symposium on Biological Complexity in La Jolla, California.

Researchers have made neurons from the skin cells of mice that model Rett syndrome, according to a study published in the December issue Molecular Psychiatry.

A new study bolsters the idea that overactive protein synthesis contributes to autism. The findings, published 21 November in Nature, show that dampening a single overabundant protein, neuroligin-1, reverses both abnormal brain activity and social deficits in mice.

Mutations in SYNGAP1, which are associated with severe intellectual disability and an increased risk of autism, do damage by speeding up the rate at which neuronal connections mature, according to a mouse study published 9 November in Cell.