Much of what we know about the underlying mechanism of ASDs comes from detailed analysis of mouse models of syndromic autism, for which a genetic cause is clearly defined. Unfortunately, while patients with these disorders frequently meet the diagnostic criteria for ASDs, autism is not always present and there are a variety of other symptoms related to abnormal brain function, making the results of these studies not necessarily generalizable to all ASDs. Nevertheless, careful review of common findings in these models contributes to a basic understanding of the pathophysiology contributing to autistic behaviors. The behavioral phenotypes in some of these ASD models have recently been reviewed in a separate paper (Bey and Jiang, 2014), so this review will focus on biochemical, cellular, and synaptic findings from select mouse models of ASDs induced by a mutation in a single gene. It should be noted that there are many models that we excluded, including inbred strains, chromosomal CNVs, and environmentally induced models, due to limited space and the fact that the biological mechanisms in these models are currently less understood. The models
