EN
Autism spectrum disorders (ASD) are a group of behaviorally defined neurodevelopmental disorders characterized with three core symptom clusters: social behavior impairments, deficient communication and in creased repetitive behaviors. The etiology of the disease remains poorly understood as many factors seem to contribute to ASD phenotype. Several mutations in genes encoding synaptic proteins have been linked with aberrant social behaviors in mouse models of autism. The condition of the synapse relies not only on the expression of these proteins but also on the state of the extracellular millieu surrounding it. The extracellular matrix (ECM) regulates formation and maturation of dendritic spines, scaffolding and presentation of growth factors to newly born neurons as well as migration of neurons and axons to their designated brain regions both during development and adulthood. The aberrant expression of its components may lead to neuropathologies observed in patients diagnosed with ASD. Here we have looked at the expression of ECM components (laminin and heparan sulfate) in the brains of BTBR T+tf/J mice, the best-studied mouse model of ASD, displaying not only behavioral deficits but also neuroanatomical features resembling those of ASD patients. We found the expression markedly decreased as compared with highly-social c57BL/6J mice, which opens an entirely new field of search for molecular basis and biomarkers of their autistic-like behaviors.