Pathological changes in synapse formation, plasticity and development are caused by altered trafficking and assembly of postsynaptic scaffolding proteins at sites of glutamatergic and gammaaminobutyric acid synapses, suggesting their involvement in the etiology of neurodevelopmental disorders, including autism. Several autism-related mouse models have been developed in recent years for studying molecular, cellular and behavioural defects to understand the etiology of autism and test potential treatment strategies. In this review, the role of alterations in selected postsynaptic scaffolding proteins in relevant transgene autism-like mouse models is explained. A summary is also provided of selected animal models by paying special attention to interactions between guanylate kinases or membrane-associated guanylate kinases, as well as other synapse protein components which form functional synaptic networks. The study of early developmental stages of autism-relevant animal models help in the understanding the origin and development of diverse autistic symptomatology.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.