INVESTIGADORES
DEPINO Amaicha Mara
congresos y reuniones científicas
Título:
Cerebellar neuroinflammation can modulate sociability in mice
Autor/es:
DEPINO AM; LUCCHINA L; KAZLAUSKAS N; CAMPOLONGO M
Lugar:
Washington DC
Reunión:
Congreso; Society for Neuroscience 2014; 2014
Institución organizadora:
Society for Neuroscience
Resumen:
Recent clinical and experimental evidence has suggested a role of the cerebellum in the etiopathogenesis of autism spectrum disorders (ASD). A brain structure generally tasked with coordinating movements, the cerebellum has been recently proved to regulate emotions and attention. To further study the role of the cerebellum in behaviors related to autism, we used a mouse model of ASD and evaluated whether histological alterations previously described in the brain of autistic individuals, could also be observed in the model. Animals exposed to valproic acid (VPA) at the gestational day (GD) 12.5, showed in adulthood signs of microgliosis in the cerebellum and an increase in the GFAP-positive area in the granular cell layer of the lobule 7. Moreover, after a peripheral LPS stimulus, the levels of pro-inflammatory cytokines were significantly increased in the cerebella of VPA mice, when compared to control mice, suggesting a primed state of glial cells in this structure. To evaluate whether cerebellar neuroinflammation could modulate behaviors related to ASD, we studied the effect on sociability after eliciting an inflammatory response specifically in the lobule 7 of the cerebellum. Animals injected with 10ng of LPS in the lobule 6/7 of the cerebellum showed a decrease in the time spent exploring a social stimulus 24 h after injection. This effect on behavior was paralleled by an activation of microglia in the region. Interestingly, the same stimulus applied to the lobules 4/5 did not affect sociability, although the increase in microglial activation was also observed. Our results suggest a role of a specific structure within the cerebellum in the regulation of sociability in mice and contribute to recent evidences highlighting the involvement of this structure in ASD.