Françoise Muscatelli

This study shows that Magel2 deficiency in a mouse model of Prader-Willi syndrome causes microglial structural changes and increased synaptic engulfment, altering neuron-microglia interactions and hypothalamic circuit function.

This study inhibits oxytocin neurons during different developmental stages in mice, revealing long-term behavioral and metabolic effects depending on timing and sex.

The paper introduces PCAN, a resource integrating high-throughput phenotyping of mouse models for Prader-Willi syndrome to evaluate phenotypes and therapeutic strategies.

This paper identifies a hypothalamus-brainstem circuit mediated by oxytocin that enhances respiratory sinus arrhythmia during calming behaviors.

The paper shows that cool thermal processing emerges in the neonatal somatosensory cortex and is disrupted in a mouse model of autism.

This study shows that oxytocin release during a neonatal critical period is essential for melanocortin circuit development and metabolic function.

This study creates a novel mouse model with deletion of Necdin and Magel2 genes, revealing functional interactions and phenotypes relevant to Prader-Willi Syndrome.

This study shows that oxytocin administration in neonatal Magel2-deficient mice restores hippocampal circuitry and social memory, suggesting therapeutic potential for autism.

This study shows that Magel2 deficiency causes reduced neurite outgrowth and glutamatergic synapses, which are partially rescued by postnatal oxytocin treatment in mice.

This study identifies early life thermosensory impairments in Magel2-deficient mice and shows oxytocin treatment can rescue these deficits.

This study shows that restoring vasopressin-oxytocin interaction in the lateral septum of Magel2 knockout mice reduces social withdrawal behavior.