CONICET | Buscador de Institutos y Recursos Humanos

Autism is a neurodevelopmental disorder characterized by the presence of stereotyped or restrictive behaviors, and impairments in communication and sociability. The exact underlying causes of this disorder are still unclear. As previous studies have shown a link between autism and neuroinflammation, our working hypothesis is that central inflammatory processes are responsible for the behavioral phenotype. Moreover, we hypothesized that there is a developmental critical window in which maturation and consolidation of the neural systems responsible for these symptoms typically occur. Using the valproic acid (VPA) model of autism, we previously detected an activated glial state in the cerebellum and the hippocampus of adult mice. The aim of this work is to identify the specific time window when inflammation appears and to study its correlation with the behavioral phenotype that we observe. We used immunofluorescence to characterize the central inflammatory state from P7 to P42. We found higher GFAP+ density and activated microglia in the hippocampus (CA1 and DG), and glial alterations in the cerebellum of VPA mice at early ages (P21 and P28). Also, we evaluated the peripheral inflammatory response and found that VPA mice have a normal corticosterone response postnatally. Our next step is to test whether modulation of the neuroinflammatory state during this critical period with an anti-inflammatory drug can revert the autism related behaviors.