ArticleGenes, brain, and behavior2020
Male-specific alterations in structure of isolation call sequences of mouse pups with 16p11.2 deletion.
Article in Genes, brain, and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- 16p11.2 duplication and NMDA receptor antagonism have distinct impacts on reward learning and decision making.Psychopharmacology · 2026Article
- 16p11.2 duplication shows early male-biased impacts on reward learning, but NMDA receptor antagonism reduces optimal choice selection in both wildtypes and 16p11.2 duplication.bioRxiv : the preprint server for biology · 2025Article
- Prenatal Exposure to Azadiradione Leads to Developmental Disabilities.Molecular neurobiology · 2025Article
- The pleiotropic spectrum of proximal 16p11.2 CNVs.American journal of human genetics · 2024Review
- Developmental encoding of natural sounds in the mouse auditory cortex.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Differential Encoding of Two-Tone Harmonics in the Male and Female Mouse Auditory Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Dissecting 16p11.2 hemi-deletion to study sex-specific striatal phenotypes of neurodevelopmental disorders.Molecular psychiatry · 2024Article
- Understanding copy number variations through their genes: a molecular view on 16p11.2 deletion and duplication syndromes.Frontiers in pharmacology · 2024Review
- Predictive Mouse Ultrasonic Vocalization Sequences: Uncovering Behavioral Significance, Auditory Cortex Neuronal Preferences, and Social-Experience-Driven Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Rodent ultrasonic vocal interaction resolved with millimeter precision using hybrid beamforming.eLife · 2023Article
- Day-to-day spontaneous social behaviours is quantitatively and qualitatively affected in a 16p11.2 deletion mouse model.Frontiers in behavioral neuroscience · 2023Article
- Temporal dynamics of isolation calls emitted by pups in environmental and genetic mouse models of autism spectrum disorder.Frontiers in neuroscience · 2023Article
- Isolation-Induced Ultrasonic Vocalization in Environmental and Genetic Mice Models of Autism.Frontiers in neuroscience · 2021Article
- 16p11.2 Copy Number Variations and Neurodevelopmental Disorders.Trends in neurosciences · 2020Review
- Male-specific alterations in structure of isolation call sequences of mouse pups with 16p11.2 deletion.Genes, brain, and behavior · 2020Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
16p11.2 deletion is one of the most common gene copy variations that increases the susceptibility to autism and other neurodevelopmental disorders. This syndrome leads to developmental delays, including speech impairment and delays in expressive language and communication skills. To study developmental impairment of vocal communication associated with 16p11.2 deletion syndrome, we used the 16p11.2del mouse model and performed an analysis of pup isolation calls (PICs). The earliest PICs at postnatal day 5 from 16p11.2del pups were found altered in a male-specific fashion relative to wild-type (WT) pups. Analysis of sequences of ultrasonic vocalizations (USVs) emitted by pups using mutual information between syllables at different positions in the USV spectrograms showed that dependencies exist between syllables in WT mice of both sexes. The order of syllables was not random; syllables were emitted in an ordered fashion. The structure observed in the WT pups was identified and the pattern of syllable sequences was considered typical for the mouse line. However, typical patterns were totally absent in the 16p11.2del male pups, showing on average random syllable sequences, while the 16p11.2del female pups had dependencies similar to the WT pups. Thus, we found that PICs were reduced in number in male 16p11.2 pups and their vocalizations lack the syllable sequence order emitted by WT males and females and 16p11.2 females. Therefore, our study is the first to reveal sex-specific perinatal communication impairment in a mouse model of 16p11.2 deletion and applies a novel, more granular method of analysing the structure of USVs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.