LONG LASTING CEREBELLAR ALTERATIONS AFTER PERINATAL ASPHYXIA IN RATS

RIVIÈRE, STÉPHANIE; CAMPANILLE, VERÓNICA; SARACENO, GUSTAVO EZEQUIEL; KOLLIKER FRES, RODOLFO; CAPANI, FRANCISCO; CASTILLA, ROCÍO

Mar del Plata, Buenos Aires

Congreso; XXX Congreso Sociedad Argentina de Investigación en Neurociencias (SAN); 2015

Sociedad Argentina de Investigación en Neurociencias

The developing brain maybe particularly vulnerable to injury before, at and after birth. Among possibleinsults, hypoxia suffered as aconsequence of perinatal asphyxia (PA) exhibits the highest incidence levelsand the cerebellar circuitry appears to be particularly susceptible, as the cellularmakeup and the quantity of inputs change quickly during days and weeksfollowing birth.In thiswork, we have used a murine model to induce severe global PA in rats at thetime of birth. Short-term cerebellar alterations within this PA model have beenpreviously reported but whether such alterations remain in adulthood has notbeen conclusively determined yet. For this reason, and given the crucialcerebellar role in determining connectivity patterns in the brain, the aim ofour work is to unveil long-term cerebellum histomorphology following a PAinsult. Morphological and cytological neuronal changes andglial reaction in the cerebellar cortex were analyzed at postnatal 120 (P120)following injury performed at birth. As compared to control, PA animalsexhibited: 1) an increase in molecular and granular thickness, both presentinglower cellular density; 2) a disarrayed Purkinje cell layer presenting a highernumber of anomalous calbindin-stained cells. 3) focal swelling andmarked fragmentation of microtubule-associated protein 2 (MAP-2) in Purkinje cell dendrites and, 4) an increasein glial fibrillary acidic protein (GFAP) expression in Bergmann cells and the granularlayer. In conclusion, we demonstrate that PA produces long-term damage incellular histomorphology in rat cerebellar cortex which could be involved inthe pathogenesis of cognitive deficits observed in both animals and humans.