ArticleThe Journal of clinical investigation2021
Correction of vasopressin deficit in the lateral septum ameliorates social deficits of mouse autism model.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Early oxytocin treatment in infants with Prader-Willi syndrome is safe and is associated with better endocrine, metabolic and behavioral outcomes.Orphanet journal of rare diseases · 2025Trial
- Oxytocin receptor signaling in the dorsal lateral septum is essential for social transmission of food preference in mice.PLoS biology · 2026Article
- Circuit logic of oxytocin and vasopressin complementary actions.Frontiers in neuroscience · 2026Review
- Neuropeptides and the Autonomic Nervous System in Prader-Willi Syndrome.International journal of molecular sciences · 2025Review
- Impaired vasopressin neuromodulation of the lateral septum leads to social behavior deficits in Shank3BNature communications · 2025Article
- Brain circuits that regulate social behavior.Molecular psychiatry · 2025Review
- Vasopressin regulates social play behavior in sex-specific ways through glutamate modulation in the lateral septum.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- MAGEL2 (patho-)physiology and Schaaf-Yang syndrome.Developmental medicine and child neurology · 2025Review
- The Hypothalamic Medial Preoptic Area-Paraventricular Nucleus Circuit Modulates Depressive-Like Behaviors in a Mouse Model of Postpartum Depression.Research (Washington, D.C.) · 2025Article
- Neuropeptide therapeutics to repress lateral septum neurons that disable sociability in an autism mouse model.Cell reports. Medicine · 2024Article
- Acute, chronic and conditioned effects of intranasal oxytocin in the mu-opioid receptor knockout mouse model of autism: Social context matters.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Hypothalamic vasopressin sex differentiation is observed by embryonic day 15 in mice and is disrupted by the xenoestrogen bisphenol A.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A vasopressin circuit that modulates mouse social investigation and anxiety-like behavior in a sex-specific manner.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- 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
- A vasopressin circuit that modulates sex-specific social interest and anxiety-like behavior in mice.bioRxiv : the preprint server for biology · 2023Article
- Biased brain and behavioral responses towards kin in males of a communally breeding species.Scientific reports · 2023Article
- Vasopressin as Possible Treatment Option in Autism Spectrum Disorder.Biomedicines · 2023Review
- The relationship between endogenous oxytocin and vasopressin levels and the Prader-Willi syndrome behaviour phenotype.Frontiers in endocrinology · 2023Article
- Modulation of social behavior by distinct vasopressin sources.Frontiers in endocrinology · 2023Review
- Linking oxytocin and arginine vasopressin signaling abnormalities to social behavior impairments in Prader-Willi syndrome.Neuroscience and biobehavioral reviews · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intellectual and social disabilities are common comorbidities in adolescents and adults with MAGE family member L2 (MAGEL2) gene deficiency characterizing the Prader-Willi and Schaaf-Yang neurodevelopmental syndromes. The cellular and molecular mechanisms underlying the risk for autism in these syndromes are not understood. We asked whether vasopressin functions are altered by MAGEL2 deficiency and whether a treatment with vasopressin could alleviate the disabilities of social behavior. We used Magel2-knockout mice (adult males) combined with optogenetic or pharmacological tools to characterize disease modifications in the vasopressinergic brain system and monitor its impact on neurophysiological and behavioral functions. We found that the activation of vasopressin neurons and projections in the lateral septum were inappropriate for performing a social habituation/discrimination task. Mechanistically, the lack of vasopressin impeded the deactivation of somatostatin neurons in the lateral septum, which predicted social discrimination deficits. Correction of vasopressin septal content by administration or optogenetic stimulation of projecting axons suppressed the activity of somatostatin neurons and ameliorated social behavior. This preclinical study identified vasopressin in the lateral septum as a key factor in the pathophysiology of Magel2-related neurodevelopmental syndromes.
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