The production, validation and study of a novel rat model for Phelan McDermid Syndrome shows an ameliorative effect of oxytocin on both social and attentional deficits.

Shank3, a high confidence autism gene candidate, may be a key component of the mechanisms underlying sleep problems in autism.

Shank promotes functional coupling between CaV1 calcium channels and BK potassium channels.

Changes in Shank gene dosage alter voltage-activated calcium current and calcium-activated gene expression in a manner that parallels the effects of human Shank copy number variation on psychiatric disease risk.

Alterations in mTOR signaling drive similar dysregulations in the critical mid-fetal neurodevelopmental processes of neurite outgrowth and cell migration in two distinct subsets of autism, idiopathic and 16p11.2 deletion.

Five mouse models of autism show deficits in delay eyeblink conditioning, a form of split-second sensory learning that involves the cerebellum, a frequent site of disruption in autistic brains.

An analysis of recent literature advances novel hypotheses and suggests new experimental approaches in order to build an integrated understanding of prefrontal neural architecture and behavioral repertoires during development.

Male and female mice differ in basal cerebellar physiology, including the magnitude of synaptic excitation by metabotropic glutamate receptors, kinetics of synaptic inhibition, intrinsic properties, and responses to autism-linked mutations.

Identifying FMRP-bound mRNAs in hippocampal CA1 pyramidal neurons reveals cell-type specific regulation of autism-candidate and circadian mRNAs and FMRP-mediated control of memory across the circadian cycle.

Autism-associated SHANK3 missense mutations result in differential protein folding, stability, and intramolecular dynamics affecting its turnover at the synapse.