16p11.2 deletion syndrome mice display sensory and ultrasonic vocalization deficits during social interactions
Open accessAbstract
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. Autism Res 2015, 8: 507–521 . © 2015 International Society for Autism Research, Wiley Periodicals, Inc.
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Startle response and pre-pulse inhibition are severely impaired in the 16p11.2+/− mice (Dolmetsch).
“Startle response [4, 60] and pre-pulse inhibition (PPI) [60] are severely impaired in the 16p11.2+/− mice (Dolmetsch).”
From 16p11.2 Copy Number Variations and Neurodevelopmental Disorders (2020) · cites this paper as [60]
These mice are deaf, which likely underlies startle/PPI deficits and may be related to altered ultrasonic vocalizations.
“However, these mice are deaf [60], which likely underlies startle/PPI deficits and may be related to altered ultrasonic vocalizations.”
From 16p11.2 Copy Number Variations and Neurodevelopmental Disorders (2020) · cites this paper as [60]
16p11.2+/− models show reduced body size/weight, in contrast to the human obesity phenotype.
“However, 16p11.2+/− models show reduced body size/weight [4, 5, 60, 61, 63], in contrast to the human obesity phenotype.”
From 16p11.2 Copy Number Variations and Neurodevelopmental Disorders (2020) · cites this paper as [60]
All three lines of 16p11.2+/− mice display social deficits in various testing paradigms and an array of cognitive deficits.
“All 3 lines of 16p11.2+/− mice display social deficits in various testing paradigms [59–64], and an array of cognitive deficits [4, 59, 62–68].”
From 16p11.2 Copy Number Variations and Neurodevelopmental Disorders (2020) · cites this paper as [60]
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- Authors
- Yang, M., Mahrt, E. J., Lewis, F., Foley, G., Portmann, T., Dolmetsch, R. E., Portfors, C. V., & Crawley, J. N.
- Affiliations
- University of California Davis Medical Center (US)
- Washington State University Vancouver (US)
- Circuit Therapeutics (United States) (US)
- Stanford Medicine (US)
- Corresponding author
- Yang, Mu
- Venue
- Autism Research
- Publisher
- Wiley
- Published
- 2015-02-07
- Volume
- 8
- Issue
- 5
- Pages
- 507-521
- ISSN
- 1939-3792 (ISSN-L)
- 1939-3806
- PMC
- PMC5321681
- OpenAlex
- W1808144476
- Cited by
- 96
- References
- 79
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 9 · 2023: 10 · 2022: 9 · 2021: 10 · 2020: 15 · 2019: 10 · 2018: 10 · 2017: 8 · 2016: 4 · 2015: 6
- FWCI
- 6.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Autism Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Simons Foundation (204340)
- National Institute of Mental Health Intramural Research Program
- National Institutes of Health Pioneer Award
- National Science Foundation (IOS 1257768)
- the Swiss National Science Foundation (PBSKP3-123434 and PA00P3_134196)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Keywords
- 16p11.2 deletion syndrome, ultrasonic vocalizations, social communication deficits, autism spectrum disorder, nociceptive threshold, acoustic startle response, hearing loss, auditory brainstem response, stereotypy, sex differences in vocalization
- MeSH terms
- Animals, Autistic Disorder, Behavior, Animal, Chromosome Deletion, Chromosomes, Human, Pair 16, Disease Models, Animal, Male, Intellectual Disability, Social Behavior, Vocalization, Animal, Chromosome Disorders, Mice
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.
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