Autism spectrum disorders (ASDs) and related neuropsychiatric diseases, such as schizophrenia, are thought to involve alterations in neural circuitry in different brain regions, including the hippocampus, an area critical for memory formation. Most studies on the role of the hippocampus in learning and memory have focused on information flow through the hippocampal CA3, CA1 and dentate gyrus subregions. Much less is known about the hippocampal CA2 region, a relatively small area that is altered in individuals with schizophrenia and bipolar disorder. The CA2 region is of particular interest in ASD because it has high levels of receptors for the social hormones oxytocin and vasopressin, which have been implicated in ASD.

Autism spectrum disorders (ASD) are strongly sex-biased. Boys are four times more likely to receive a diagnosis than girls, with ASDs affecting an estimated 1 in 42 males in the U.S. The biological mechanisms contributing to these sex differences are currently unknown.

A common feature of mouse models of autism spectrum disorders (ASDs) is an imbalance between excitation and inhibition within circuits of the central nervous system. This imbalance is thought to contribute to disrupted neural function in these disorders, but the ultimate cause of this imbalance remains unclear.

The core social impairments that characterize autism spectrum disorder (ASD) remain poorly understood. Improved understanding of ASD has been hindered by the inability to directly study brain tissue in ASD patients, and mice lack the complex social capabilities found in humans and other primates. These limitations have impeded the discovery of ASD biomarkers and the development of promising medications to treat social deficits seen in ASD.

Autism spectrum disorders (ASDs) are genetically heterogeneous, but whether they share a common neural-circuit-processing defect is unclear. One hypothesis is that the ratio of excitation to inhibition (the E/I ratio) in the brain's cerebral cortex is elevated in ASDs. Elevations in this ratio could cause hyperexcitability of neural circuits, leading to impaired information processing and hypersensitivity to sensory stimuli, features commonly seen in individuals with ASD.

Autism can be thought of as a dysfunction in the interaction between cortical areas, particularly the top-down interactions that enable us to select features of our environment that are relevant for the task at hand and to suppress features that are task-irrelevant. Charles Gilbert and his colleagues at Rockefeller University propose a combination of behavioral and high-resolution imaging experiments to study the mechanisms of autism at the level of the circuitry of the cerebral cortex in animal models of autism.

Animal models play pivotal roles in understanding the relationship between behaviors and underlying brain circuits. One of the key features of autism is a deficit in social communication, including vocal communication. The primary animal models for autism research have been rodents because of the advantage of genetic manipulations. However, rodents lack certain social communication behaviors exhibited by primates, such as eye contact and high-level vocal communication. There is therefore a great need to develop new animal models, preferably nonhuman primate models, for autism research.

A core feature of autism is the expression of repetitive and ritualized behaviors characterized by profound invariability and inflexibility. Autism is also frequently comorbid with anxiety disorders. Despite intensive study, the mechanisms underlying the repetitive and ritualized behavior in autism and the high prevalence of comorbidity between autism and anxiety disorders remain largely unknown.

The sense of touch allows us to navigate our physical world. The first step in tactile processing involves the activation of low-threshold mechanoreceptor neurons (LTMRs) with highly specialized endings in the skin. Social (affective) touch may be mediated by a unique class of slowly conducting C-fibers, the C-LTMRs.