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Exogenous and evoked oxytocin restores social behavior in the Cntnap2 mouse model of autism
Open accessAbstract
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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In the citing paper
“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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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
In the citing paper
“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
In the citing paper
“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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Metadata
- 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
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › 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
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