M6a glycoprotein is involved in neuronal plasticity after perinatal asphyxia.

SARACENO EZEQUIEL; BROCCO MARCELA ADRIANA; GALEANO PABLO; ROMERO JUAN I; HOLUBIEC MARIANA; CAPANI FRANCISCO

Huerta Grande-Córdoba

Congreso; I Reunión Conjunta de Neurociencias (IRCN); 2009

During perinatal asphyctic episode (PA), synaptic dysfunction observed has been related with neuronal death, although this mechanism is not fully understood yet. In previous work we have shown the effects of PA on the actin cytoskeleton of neostriatal and hippocampal post-synaptic densities (PSD) in 30 days old rats. Therefore, we observed that the number of dendritic spines in both areas increased in animals that suffered PA. In this work, we study the effects of PA on the neuronal plasticity of the central nervous system (CNS). To this propose, we analyzed the glycoprotein M6a, involved in hippocampal neuronal plasticity under a stress episode inducing neurites formation and increase filopodium/spines density, by inmunofluorescent technique and Real Time PCR in 30 days old rats. Staining with M6a antibody followed by fluorescent microscopy analysis showed an increase of M6a fluorescent staining in neostriatal and CA1 hippocampal slices (ESTADISTICA). Real time PCR revealed an over expression of M6a gene in hippocampal area (ESTADISTICA), but in neostriatum an over expression was not observed (ESTADISTICA). These results suggest that M6a glycoprotein will be involve in the dynamic of dendritic spines in asphyctic animals. Therefore, provided that filopodium/spines formation is related with synapses formation and stabilization, M6a could play a role in the synapses establishment.