The cerebellum, a brain region long established to have a role in motor control, has begun to be appreciated for its involvement in sensory perception and higher cognitive functions. Our previous research has found evidence for a prostaglandin E2 (PGE2)-estradiol signaling pathway in the rat cerebellum, and decreasing PGE2 synthesis in the second postnatal week results in excessive growth of Purkinje cell dendritic trees and abnormal sensory and social behavior. Here we confirm that this signaling pathway has a role in Purkinje cell development by demonstrating that during the second postnatal week, inducing an increase in PGE2 synthesis by treatment with lipopolysaccharide (LPS) increases aromatase activity and estradiol synthesis and stunts Purkinje cell dendrite growth. Additionally, we report that inflammation induced by LPS or mimicked by directly injecting PGE2 disrupts social and cognitive behaviors without affecting normal motor control. Specifically, in males and females, both LPS and PGE2 increase total object exploration, which we interpret as increased perseverance of interest with objects. LPS and PGE2 also decrease social play behavior, but only in males. These changes in Purkinje cell development and in behavior can be prevented with the aromatase inhibitor, formestane, suggesting a link between estradiol, cerebellar development, and its role in higher cognitive functioning. Further, these biochemical, morphological, and behavioral changes are only seen when inflammation occurs within the second postnatal week, not in the first or third. Autism spectrum disorder and Schizophrenia are neurodevelopmental diseases with complex and poorly understood genetic and environmental components. Both have been associated with cerebellar pathology and early life inflammation, particularly the developmental period between in utero and early childhood - a very similar time frame to the sensitive period we describe. Our findings suggest that the second postnatal week of life in the rat is a developmental period in which fever and inflammation may increase the risk for neurodevelopmental disorders by altering cerebellar development.