ArticleAutism research : official journal of the International Society for Autism Research2015
16p11.2 Deletion Syndrome Mice Display Sensory and Ultrasonic Vocalization Deficits During Social Interactions.
Article in Autism research : official journal of the International Society for Autism Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.
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Who cites it
60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 97 citations in OpenAlex.
- A systematic review and meta-analysis of how social memory is studied.Scientific reports · 2024Pooled it
- Auditory processing in rodent models of autism: a systematic review.Journal of neurodevelopmental disorders · 2022Pooled it
- Cerebellar pathology contributes to neurodevelopmental deficits in spinal muscular atrophy.Brain : a journal of neurology · 2026Article
- Hidden in plain sound: the scientific potential of house mouse squeaks.Biology letters · 2025Review
- Neurocognitive profiles of 22q11.2 and 16p11.2 deletions and duplications.Molecular psychiatry · 2025Article
- The pleiotropic spectrum of proximal 16p11.2 CNVs.American journal of human genetics · 2024Review
- Adenosine mediates the amelioration of social novelty deficits during rhythmic light treatment of 16p11.2 deletion female mice.Molecular psychiatry · 2024Article
- Article
- Understanding copy number variations through their genes: a molecular view on 16p11.2 deletion and duplication syndromes.Frontiers in pharmacology · 2024Review
- A Novel Head-Fixed Assay for Social Touch in Mice Uncovers Aversive Responses in Two Autism Models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- 16p11.2 deletion mice exhibit compromised fronto-temporal connectivity, GABAergic dysfunction, and enhanced attentional ability.Communications biology · 2023Article
- Sleep disturbances in autism spectrum disorder: Animal models, neural mechanisms, and therapeutics.Neurobiology of sleep and circadian rhythms · 2023Review
- The molecular pathology of schizophrenia: an overview of existing knowledge and new directions for future research.Molecular psychiatry · 2023Review
- Day-to-day spontaneous social behaviours is quantitatively and qualitatively affected in a 16p11.2 deletion mouse model.Frontiers in behavioral neuroscience · 2023Article
- Sensory processing in 16p11.2 deletion and 16p11.2 duplication.Autism research : official journal of the International Society for Autism Research · 2022Article
- Histone Deacetylase Inhibition Restores Behavioral and Synaptic Function in a Mouse Model of 16p11.2 Deletion.The international journal of neuropsychopharmacology · 2022Article
- Beyond the three-chamber test: toward a multimodal and objective assessment of social behavior in rodents.Molecular autism · 2022Review
- Prefrontal circuits guiding social preference: Implications in autism spectrum disorder.Neuroscience and biobehavioral reviews · 2022Review
- Social behavior in 16p11.2 and 22q11.2 copy number variations: Insights from mice and humans.Genes, brain, and behavior · 2022Review
- Understanding autism spectrum disorders with animal models: applications, insights, and perspectives.Zoological research · 2021Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Recurrent deletions and duplications at chromosomal region 16p11.2 are variably associated with speech delay, autism spectrum disorder, developmental delay, schizophrenia, and cognitive impairments. Social communication deficits are a primary diagnostic symptom of autism. Here we investigated ultrasonic vocalizations (USVs) in young adult male 16p11.2 deletion mice during a novel three-phase male-female social interaction test that detects vocalizations emitted by a male in the presence of an estrous female, how the male changes its calling when the female is suddenly absent, and the extent to which calls resume when the female returns. Strikingly fewer vocalizations were detected in two independent cohorts of 16p11.2 heterozygous deletion males (+/-) during the first exposure to an unfamiliar estrous female, as compared to wildtype littermates (+/+). When the female was removed, +/+ emitted calls, but at a much lower level, whereas +/- males called minimally. Sensory and motor abnormalities were detected in +/-, including higher nociceptive thresholds, a complete absence of acoustic startle responses, and hearing loss in all +/- as confirmed by lack of auditory brainstem responses to frequencies between 8 and 100 kHz. Stereotyped circling and backflipping appeared in a small percentage of individuals, as previously reported. However, these sensory and motor phenotypes could not directly explain the low vocalizations in 16p11.2 deletion mice, since (a) +/- males displayed normal abilities to emit vocalizations when the female was subsequently reintroduced, and (b) +/- vocalized less than +/+ to social odor cues delivered on an inanimate cotton swab. Our findings support the concept that mouse USVs in social settings represent a response to social cues, and that 16p11.2 deletion mice are deficient in their initial USVs responses to novel social cues.
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