The term "Autism Spectrum" is often used to describe disorders that are currently classified as Pervasive Developmental Disorders.
These disorders are typically characterized by social deficits, communication difficulties, stereotyped or repetitive behaviors
and/or cognitive delays or mental retardation; sometimes they present high comorbidity rates with epilepsy. Although these diagnoses
share some common features, individuals with these disorders are thought to be "on the spectrum" because of differences in severity
across these domains.
Recent advances in the genetics of autism spectrum disorders (ASDs) are offering new valuable insights into molecular and cellular
mechanisms of pathology. Of particular interest are transgenic technologies that allowed the engineering of several mouse models mimicking
different kinds of monogenic heritable forms of ASDs. These transgenic models provide excellent opportunities to explore in detail
cellular and molecular mechanisms underlying disease pathology and to identify novel targets for therapeutic intervention.
Increasing evidence suggests that the pathophysiological core of the murine model is primarily due to changes in normal synaptic transmission
Here, we will extensively review the synaptic alterations across different animal models of ASDs and recapitulate the pharmacological
strategies aimed at rescuing hippocampal plasticity phenotypes. We describe how pharmacological modulation of mGlu5 receptor,
through the use of positive or negative allosteric modulators (depending on the specific disorder), may represent a promising therapeutic
strategy for ASDs treatment.