Oxytocin actions of prefrontal cortex circuits in a mouse model of Prader-Willi Syndrome

Mental illness is a major problem in Prader-Willi syndrome (PWS). It prevents social interactions and seriously threatens the quality of life of the patient and of those around the patient. Mood swings, stereotyped repetitive behaviors, psychotic episodes are dependent on proper functioning of brain regions such as the prefrontal cortex. Activity in the prefrontal cortex also contributes to the feeling of satiety after food intake. Oxytocin, a signaling molecule present in the brain is important for social communication, self control, trust and for sustaining normal mental functions. Oxytocin is also important for controlling satiety after food intake. The number of oxytocin neurons is reduced in the brain of PWS subjects as well as in the Magel2 mouse model of PWS. The reduced oxytocin levels may contribute to the mental deficits and hyperphagia in PWS patients. Intranasal oxytocin, that increases activity in the prefrontal cortex, reduces autistic and psychotic symptoms in patients. Whether normal oxytocin signaling is retained in the prefrontal cortex in the absence of Magel2 is not known. Using living brain tissue from normal and Magel2-deficient mice, we will use sophisticated methods to monitor the activity of prefrontal cortical neurons to determine if their response to oxytocin is altered in Magel2 null mutants. These studies will help determine if the cortex is able to respond normally to oxytocin in Magel2 mice and provide guidance for developing oxytocin and/or other therapeutic tools for treating psychiatric and eating dysfunctions in PWS subjects

Funded Year:


Awarded to:

Meenakshi Alreja, PhD


$108,000 (OSS Funds)


Yale University

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