DESCRIPTION

Oxytocin contributes to regulate the cytoskeletal and synaptic proteins and could also affect the mechanisms of neurodevelopmental disorders, such as autism.

Both the Prader-Willi syndrome and Schaaf-Yang syndrome exhibit autistic symptoms involving the
MAGEL2 gene.

Magel2-deficient mice show a deficit in social behavior that is rescued following several administration of oxytocin.

Here, in Magel2-deficient mice, we showed that the neurite outgrowth of primary cultures of immature hippocampal neurons is reduced.

The treatment with oxytocin can reverse this abnormality.

In the hippocampus of Magel2-deficient pups, we demonstrated that several transcripts of neurite
outgrowth-associated proteins, synaptic vesicle proteins, and cell-adhesion molecules are decreased.

In the juvenile stage, when neurons are mature, normalization or even overexpression of most of these markers was observed, suggesting a delay in the neuronal maturation.

Then, we found reduced transcripts of the excitatory postsynaptic marker, Psd95 in the hippocampus and we observed a decrease of PSD95/VGLUT2 colocalization in the hippocampal CA1 and CA3 regions in Magel2-deficient mice, indicating a defect in glutamatergic synapses.

The Postnatal administration of oxytocin upregulated postsynaptic transcripts in pups; however, it did not restore the level of markers of glutamatergic synapses in Magel2-deficient mice.

In conclusion, Magel2 leads to abnormal neurite outgrowth and reduced glutamatergic synapses during development, suggesting abnormal neuronal maturation.

Oxytocin stimulates the expression of genes involved in neurite outgrowth and synapse formation in the first stages of life.

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