Enriched Environment Mitigates Cerebellar and Sensorimotor Deficits After Perinatal Asphyxia in Rats: A Correlative Morphological and Behavioral Study

Perinatal asphyxia (PA) is a major cause of neonatal brain injury and long-term neurodevelopmental impairment. Although no specific treatment exists, early-life exposure to an enriched environment (EE) has been proposed as a non-pharmacological strategy to enhance neuroplasticity and functional recovery. The main objective of this work is to evaluate whether EE mitigates cerebellar alterations and sensorimotor deficits induced by PA in a rat model. Newborn rats were assigned to control or PA groups and housed under standard (ST) or enriched (EE) conditions until postnatal day 21. Cerebellar morphology was assessed using GFAP, MAP-2, and neurofilament immunolabeling [1,2]. Early sensorimotor reflexes—including righting, air-righting, limb grasp, walking, and negative geotaxis—were evaluated [3-5], PA-ST animals showed disrupted Bergmann glia organization and reduced molecular layer thickness, both partially restored in PA-EE. GFAP reactivity increased in CTL-EE and PA-EE (p < 0.001), indicating astroglial activation. MAP-2 expression decreased in PA-ST and PA-EE (p < 0.001), with denser labeling near Purkinje cells. Behaviorally, PA-ST rats exhibited significant impairments across multiple reflexes, while EE exposure improved or normalized performance, reaching control levels in several tasks. Therefore, early exposure to an enriched environment attenuates PA-induced cerebellar alterations and sensorimotor deficits. These findings support EE as a promising early intervention strategy for neonatal brain injury. In addition, the morphological analysis together with behavioral test are a relevant methodology to assess a novel therapeutical tool for PA