Rescue of oxytocin response and social behaviour in a mouse model of autism
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A fundamental challenge in developing treatments for autism spectrum disorders is the heterogeneity of the condition. More than one hundred genetic mutations confer high risk for autism, with each individual mutation accounting for only a small fraction of cases 1-3. Subsets of risk genes can be grouped into functionally related pathways, most prominently those involving synaptic proteins, translational regulation, and chromatin modifications. To attempt to minimize this genetic complexity, recent therapeutic strategies have focused on the neuropeptides oxytocin and vasopressin 4-6, which regulate aspects of social behaviour in mammals 7. However, it is unclear whether genetic risk factors predispose individuals to autism as a result of modifications to oxytocinergic signalling. Here we report that an autism-associated mutation in the synaptic adhesion molecule Nlgn3 results in impaired oxytocin signalling in dopaminergic neurons and in altered behavioural responses to social novelty tests in mice. Notably, loss of Nlgn3 is accompanied by a disruption of translation homeostasis in the ventral tegmental area. Treatment of Nlgn3-knockout mice with a new, highly specific, brain-penetrant inhibitor of MAP kinase-interacting kinases resets the translation of mRNA and restores oxytocin signalling and social novelty responses. Thus, this work identifies a convergence between the genetic autism risk factor Nlgn3, regulation of translation, and oxytocinergic signalling. Focusing on such common core plasticity elements might provide a pragmatic approach to overcoming the heterogeneity of autism. Ultimately, this would enable mechanism-based stratification of patient populations to increase the success of therapeutic interventions.
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Neuroligin3 (Nlgn3)-knockout mice showed impaired social memory, but this seemed due to the insensitivity of VTA dopamine neurons to oxytocin even when applied exogenously.
“Somewhat differently, neuroligin3 (Nlgn3)-knockout mice also showed impaired social memory, but this seemed due to the insensitivity of VTA dopamine neurons to oxytocin even when applied exogenously”
From Oxytocin, Neural Plasticity, and Social Behavior (2021) · cites this paper as Hörnberg et al. 2020
In another autism spectrum disorder mouse model, OXTR signaling in ventral tegmental area dopamine neurons, which mediate social reward, is disrupted, and a kinase inhibitor that restores OXTR signaling also restores disrupted ASD-relevant social behaviors.
“In another ASD mouse model, OXTR signaling in VTA dopamine neurons, which mediate social reward, is disrupted, and a kinase inhibitor that restores OXTR signaling also restores disrupted ASD-relevant social behaviors (161).”
From Oxytocin, Vasopressin, and Social Behavior: From Neural Circuits to Clinical Opportunities (2022) · cites this paper as [161]
Restoration of oxytocin signaling in the VTA in an autism spectrum disorder-related mouse model was sufficient to rescue social novelty responses.
“Furthermore, restoration of oxytocin signaling in the VTA in an autism spectrum disorder-related mouse model was sufficient to rescue social novelty responses (Hörnberg et al., 2020).”
From Oxytocin neurons mediate the effect of social isolation via the VTA circuits (2022) · cites this paper as Hörnberg et al., 2020
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- Authors
- Hörnberg, H., Pérez-Garci, E., Schreiner, D., Hatstatt-Burklé, L., Magara, F., Baudouin, S., Matter, A., Nacro, K., Pecho-Vrieseling, E., & Scheiffele, P.
- Affiliations
- University of Basel (CH)
- Centre Hospitalier Universitaire Vaudois (CH)
- Experimental Drug Development Centre (SG)
- Corresponding author
- Scheiffele, Peter
- Venue
- Nature
- Published
- 2020-08-05
- Volume
- 584
- Issue
- 7820
- Pages
- 252-256
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC7116741
- OpenAlex
- W3047544314
- Cited by
- 154
- References
- 64
- Citations by year
- 2026: 13 · 2025: 25 · 2024: 28 · 2023: 24 · 2022: 28 · 2021: 31 · 2020: 5
- FWCI
- 24.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (acceptedVersion)
- PubMed Central (acceptedVersion)
- SERVAL (Université de Lausanne) (acceptedVersion, other-oa)
- IRIS (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (submittedVersion)
- edoc (University of Basel) (submittedVersion)
- Funders
- National Science Foundation
- Autism Speaks
- European Federation of Pharmaceutical Industries and Associations (777394, AIMS-2-TRIALS)
- Simons Foundation Autism Research Initiative
- European Commission (HORIZON2020, 777394)
- Agency for Science, Technology and Research (11 03 FG 07 05)
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (140944, 160319)
- Topics
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- autism spectrum disorder, neuroligin-3, dopaminergic neurons, ventral tegmental area, social behavior, synaptic adhesion molecules, translational regulation, autism heterogeneity
- MeSH terms
- Animals, Autistic Disorder, Disease Models, Animal, Male, Membrane Proteins, Mice, Inbred C57BL, Nerve Tissue Proteins, Neurons, Oxytocin, Phosphorylation, RNA, Messenger, Social Behavior, Protein Biosynthesis, Signal Transduction, Cell Adhesion Molecules, Neuronal, Ventral Tegmental Area, Mice, Knockout, Mitogen-Activated Protein Kinases, Eukaryotic Initiation Factor-4E, Mice
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