Exogenous and evoked oxytocin restores social behavior in the Cntnap2 mouse model of autism
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Mice carrying a genetic mutation that causes autistic symptoms show improved sociability after being treated with oxytocin, a hormone promoting mothering and trust.
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Melanocortin receptor agonists mimic the prosocial effects of OT in a mouse model of autism.
“mimic the prosocial effects of OT in a mouse model of autism (41)”
From Statistical and Methodological Considerations for the Interpretation of Intranasal Oxytocin Studies (2016) · cites this paper as [41]
Cntnap2−/− mice show abnormal migration of neurons in the corpus callosum and somatosensory cortex, have fewer parvalbumin-immunoreactive interneurons in the hippocampus and striatum, fewer GABAergic interneurons in the somatosensory cortex, and fewer oxytocin-expressing neurons in the hypothalamic paraventricular nucleus.
“When compared to WT controls, Cntnap2−/− mice show abnormal migration of neurons in the corpus callosum and somatosensory cortex, have fewer parvalbumin-immunoreactive interneurons in the hippocampus and striatum, fewer GABAergic interneurons in the somatosensory cortex [278] and fewer oxytocin-expressing neurons in the hypothalamic paraventricular nucleus [279].”
From Autism spectrum disorder: neuropathology and animal models (2017) · cites this paper as [279]
Altered levels of OXT and OXTR in specific brain regions have been reported in animal models of psychiatric and neurodevelopmental disorders.
“Altered levels of OXT and OXTR in specific regions of the brain have been reported in a number of animal models of psychiatric and neurodevelopmental disorders [116-119].”
From Oxytocin Signaling in the Central Amygdala Modulates Emotion Discrimination in Mice (2019) · cites this paper as [118]
Hypothalamic disruptions of OT neurons have been reported in human patients with ASD related disorders and in knockout mice for ASD risk genes including Fmr1, Cntnap2, and Pten.
“hypothalamic disruptions of OT neurons have been reported in human patients with ASD related disorders such as Prader Willi syndrome (Swaab et al., 1995), as well as in knockout mice for ASD risk genes including Fmr1 (Francis et al., 2014), Cntnap2 (Peñagarikano et al., 2015), and Pten (Page et al., 2009)”
From Parallel social information processing circuits are differentially impacted in autism (2020) · cites this paper as Peñagarikano et al., 2015
Accumulating evidence from mouse models of autism suggests that stimulating oxytocin neurons can rescue social deficits.
“Indeed, accumulating evidence from mouse models of autism suggests that stimulating oxytocin neurons can rescue social deficits.”
From Translational opportunities for circuit-based social neuroscience: advancing 21st century psychiatry (2021) · cites this paper as [29]
Chemogenetic stimulation of oxytocin neurons or pharmacologically-evoked release of endogenous oxytocin rescues social deficits in Cntnap2 knockout mice.
“while chemogenetic stimulation of oxytocin neurons or pharmacologically-evoked release of endogenous oxytocin rescues the deficits [29].”
From Translational opportunities for circuit-based social neuroscience: advancing 21st century psychiatry (2021) · cites this paper as [29]
Cntnap2 knockout mice show deficits in social behavior and reduced numbers of oxytocin neurons.
“Cntnap2 knockout mice show deficits in social behavior and reduced numbers of oxytocin neurons”
From Translational opportunities for circuit-based social neuroscience: advancing 21st century psychiatry (2021) · cites this paper as [29]
Cntnap2 knockout mice display social deficits in addition to epilepsy and cortical dysplasia and show a reduction in neurons expressing OT in the PVN.
“These mice display social deficits in addition to epilepsy and cortical dysplasia and show a reduction in neurons expressing OT in the PVN.”
From A precision medicine approach to oxytocin trials (2017) · cites this paper as Penagarikano et al. 2015
Daily chronic intranasal administration of OT early in life (between P7 and P21) in Cntnap2 knockout mice rescues their social interest and social approach.
“Also, daily chronic intranasal administration of OT early in life (between P7 and P21) in Cntnap2 knockout mice rescues their social interest and social approach.”
From A precision medicine approach to oxytocin trials (2017) · cites this paper as Penagarikano et al. 2015
Chronic exogenous OT administration to Cntnap2 knockout mice, a mouse model of autism, rescues their social deficits.
“More recently, researchers showed that chronic exogenous OT administration to Cntnap2 knockout mice, a mouse model of autism, rescues their social deficits (Penagarikano et al. 2015).”
From A precision medicine approach to oxytocin trials (2017) · cites this paper as Penagarikano et al. 2015
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- Authors
- Peñagarikano, O., Lázaro, M. T., Lu, X.-H., Gordon, A., Dong, H., Lam, H. A., Peles, E., Maidment, N. T., Murphy, N. P., Yang, X. W., Golshani, P., & Geschwind, D. H.
- Affiliations
- University of California, Los Angeles (US)
- Weizmann Institute of Science (IL)
- Corresponding author
- Geschwind, Daniel H.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2015-01-21
- Volume
- 7
- Issue
- 271
- Pages
- 271ra8-271ra8
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC4498455
- OpenAlex
- W2097364496
- Cited by
- 378
- References
- 77
- Citations by year
- 2026: 19 · 2025: 23 · 2024: 31 · 2023: 34 · 2022: 32 · 2021: 43 · 2020: 24 · 2019: 36 · 2018: 32 · 2017: 43 · 2016: 36 · 2015: 25
- FWCI
- 74.73
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- NIH (NIH/NS50220)
- National Institute of Mental Health (NIMH) (R01 MH081754-02R)
- NIH/National Institute of Neurological Disorders and Stroke (NINDS) (R01 NS049501, R01 NS074312)
- Autism Speaks
- Simons Foundation Autism Research Initiative
- McKnight Foundation
- NIH Autism Centers of Excellence (ACE) (1P50-HD055784-01)
- Network (5R01-MH081754-04)
- UCLA Center for Autism Research and Treatment (CART) Pilot
- 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
- oxytocin, CNTNAP2, autism spectrum disorder, social behavior deficits, paraventricular nucleus, oxytocin neurons, DREADD, drug screening
- MeSH terms
- Animals, Animals, Newborn, Autistic Disorder, Behavior, Animal, Disease Models, Animal, Humans, Membrane Proteins, Mice, Mutant Strains, Nerve Tissue Proteins, Neurons, Oxytocin, Paraventricular Hypothalamic Nucleus, Social Behavior, Mice, Knockout
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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