V-076
Enriched Environment Modulates Glial Reactivity and Restores Cerebellar Function After Perinatal Asphyxia in Rats
Marcos Vinícius D'Ambrósio Andrade1,2, Tamara Kobiec1,3, Anna Zeren1, Kelly Cristina de Brito Oliveira1,2, Demilson Andres Huerta Encina1,2, Paloma Martinez Cartier1, Agustina Belen Santos1, Juan Pablo Luaces1, Francisco Capani1,3
  1. Centro de Altos Estudios en Ciencias Humanas y de la Salud. Universidad Abierta Interamericana, Buenos Aires, Argentina
  2. Facultad de Medicina, Fundación H. A. Barceló. Buenos Aires, Argentina
  3. Facultad de Psicología y Psicopedagogía, Universidad Católica Argentina, Buenos Aires, Argentina
Presenting Author:
Marcos Vinícius D'Ambrósio Andrade
mvinicius309@gmail.com
Perinatal asphyxia (PA), caused by impaired placental gas exchange during gestation or delivery, increases the risk of neonatal brain injury and long-term neurodevelopmental disorders. Although no specific therapy exists, non-pharmacological interventions such as Enriched Environment (EE) have shown promise in promoting neuroplasticity and functional recovery. This study evaluated the effects of EE on cerebellar morphology and sensorimotor reflexes in PA-exposed rats. Newborn rats were assigned to control and PA groups, housed under standard (ST) or enriched (EE) conditions until postnatal day 21. Cerebellar tissue was analyzed using GFAP, MAP-2, and NF markers. PA-ST animals showed altered Bergmann glia and reduced molecular layer thickness, partially restored in PA-EE. GFAP reactivity was elevated in both CTL-EE and PA-EE (p < 0.001), suggesting astroglial activation. MAP-2 expression was decreased in PA-ST and PA-EE (p < 0.001), with denser labeling near Purkinje cells. Behaviorally, PA-ST rats exhibited significant deficits in righting (p < 0.05), air righting (p < 0.001), limb grasp (p < 0.001), walking (p < 0.05), and negative geotaxis (p < 0.05). EE exposure improved or normalized these reflexes, reaching control levels in several tasks. These findings support EE as a promising early intervention strategy to mitigate PA-induced cerebellar damage and functional impairments.