Ricerc@Sapienza

Autism Spectrum Disorders (ASDs) are neurodevelopmental syndromes, characterized by behavioral deficits and a strong genetic background.
In the last decades, the synaptic pathway has been identified as one of the affected molecular signaling cascades in these disorders. Indeed, the communication among presynaptic and postsynaptic terminals is crucial for establishing proper synaptic function and animal behavior.
Neuroligin and dystrophin both act on the establishment of functional synapses. We propose to analyze glucocorticoids treatments in two mice models, one with a mutation in Neuroligin3 and the other with a deletion of dystrophin. Both animal models exhibit behavioral deficit having manifestations characteristic of ASDs. We propose to analyse the effects of glucocorticoids treatment on the molecular pathways involved in the glucocorticoid receptors signaling in the cerebellum and on the behaviour of mdx and R451C Neuroligin 3 mice, after subchronic DEX treatment, using tests known to be dependent on cerebellar integrity.