Linking oxytocin and arginine vasopressin signaling abnormalities to social behavior impairments in Prader-Willi syndrome.

Prader-Willi syndrome (PWS) is a genetic neurodevelopmental disorder. Global hypothalamic dysfunction is a core feature of PWS and has been implicated as a driver of many of PWS's phenotypic characteristics (e.g., hyperphagia-induced obesity, hypogonadism, short stature). Although the two neuropeptides (i.e., oxytocin [OXT] and arginine vasopressin [AVP]) most implicated in mammalian prosocial functioning are of hypothalamic origin, and social functioning is markedly impaired in PWS, there has been little consideration of how dysregulation of these neuropeptide signaling pathways may contribute to PWS's social behavior impairments. The present article addresses this gap in knowledge by providing a comprehensive review of the preclinical and clinical PWS literature–spanning endogenous neuropeptide measurement to exogenous neuropeptide administration studies–to better understand the roles of OXT and AVP signaling in this population. The preponderance of evidence indicates that OXT and AVP signaling are indeed dysregulated in PWS, and that these neuropeptide pathways may provide promising targets for therapeutic intervention in a patient population that currently lacks a pharmacological strategy for its debilitating social behavior symptoms. • Prader-Willi syndrome has global hypothalamic dysfunction and social deficits. • Hypothalamic oxytocin and vasopressin signaling are critical for social function. • Oxytocin and vasopressin signaling are abnormal in Prader-Willi syndrome. • Oxytocin or vasopressin administration improves social function in animal models. • These pathways may be therapeutic targets for Prader-Willi syndrome social deficits. [ABSTRACT FROM AUTHOR]