it difficult to establish a link between synaptic dysfunction and behavioral impairments. These challenges thus demand a shift from the current analytic paradigm that combines behavior, synaptic electrophysiology, and biochemical approaches. We propose that an analytic paradigm that integrates the behavior and in vivo physiological recordings in multiple sites is a more productive approach to model autism in mice. Furthermore, manipulation of ASD candidate genes spatially and temporally will further delineate the circuits underlying ASDs. In the future, manipulation of the genomes in other species such as rat or non-human primate models may overcome the many limitations of mouse models. A more complete understanding of the current genetic models of ASDs will allow researchers to study the role of non-genetic factors and their biological underpinnings. Ultimately, knowledge learned from animal models will lead to the development of effective clinical intervention that targets the specific molecular pathways and neural circuits.
