<p><b>The neurodevelopmental condition autism spectrum disorder (ASD) is marked by impaired communication, impaired social interaction, and repetitive or restricted behaviours (American Psychiatric Association, 2013). ASD is caused by a combination of genetic and environmental factors, including maternal infection during pregnancy. There are no pharmacological treatment options for ASD, but environmental enrichment (EE) is a promising alternative to rehabilitate or prevent related symptoms. Patients with ASD often have a deficit in higher social abilities, including prosociality, but to date, no rat studies have investigated how EE affects higher social functions in the context of ASD. Therefore, this thesis investigated the effect of EE on higher social functions in an in vivo rodent model of ASD. Using a two-by-two factorial design, pregnant Sprague Dawley rats received either saline or the viral mimic polyinosinic-polycytidylic acid (poly I:C) to trigger an immune reaction and were placed in either standard or enriched housing. In the enrichment groups, pups received pre-weaning enrichment sessions while animals in the standard-housing groups were left undisturbed until weaning. I assessed the animals’ neonatal communication, general sociability and social novelty behaviour, prosocial tendencies, and locomotor activity. The main hypothesis I investigated was that the maternal immune reaction would disrupt fetal neural development and alter communication and social behaviours in the offspring and that EE would reduce or reverse these deficits. </b></p><p>There was a transient poly I:C effect on neonatal communication early on, but the treatment did not cause long-term social deficits. Poly I:C also affected adult locomotor activity but did neither reduce sociability nor prosociality. As the very weak treatment effects did not result in clear deficits, EE could not lead to improvements. While the findings did not offer insight into the enrichment effect on impaired prosocial behaviours, this was likely due to methodological issues and limitations. Future ASD research should address these concerns to further the understanding of how environmental adjustments can stimulate the impaired social parts of the brain to redirect the atypical developmental trajectory towards a more typical one.</p>