ReviewNeuroscience and biobehavioral reviews2022
Linking oxytocin and arginine vasopressin signaling abnormalities to social behavior impairments in Prader-Willi syndrome.
Review in Neuroscience and biobehavioral reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Somatostatin-expressing interneurons of prefrontal cortex modulate social deficits in the Magel2 mouse model of autism.Molecular autism · 2025Article
- Oxytocin in neurodevelopmental disorders: Autism spectrum disorder and Prader-Willi syndrome.Pharmacology & therapeutics · 2024Review
- Disengagement of somatostatin neurons from lateral septum circuitry by oxytocin and vasopressin restores social-fear extinction and suppresses aggression outbursts in Prader-Willi syndrome model.Biological psychiatry · 2024Article
- The Pivotal Role of Oxytocin's Mechanism of Thermoregulation in Prader-Willi Syndrome, Schaaf-Yang Syndrome, and Autism Spectrum Disorder.International journal of molecular sciences · 2024Review
- Tales from the life and lab of a female social neuroscientist.Comprehensive psychoneuroendocrinology · 2023Review
- Oxytocin's Regulation of Thermogenesis May Be the Link to Prader-Willi Syndrome.Current issues in molecular biology · 2023Review
- Individual differences in social homeostasis.Frontiers in behavioral neuroscience · 2023Review
- Intranasal Oxytocin in Pediatric Populations: Exploring the Potential for Reducing Irritability and Modulating Neural Responses: A Mini Review.Journal of psychiatry and brain science · 2023Article
- The relationship between endogenous oxytocin and vasopressin levels and the Prader-Willi syndrome behaviour phenotype.Frontiers in endocrinology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.