ArticleCell reports2014
Behavioral abnormalities and circuit defects in the basal ganglia of a mouse model of 16p11.2 deletion syndrome.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 2 of them syntheses that pooled it.
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Who cites it
155 citing papers in PubMed, 2 syntheses or guidelines pooled it, 261 citations in OpenAlex.
- A systematic review and meta-analysis of the relationship between genes and reflexive attention.Frontiers in neuroscience · 2025Pooled it
- The functional neural architecture of dysfunctional reward processing in autism.NeuroImage. Clinical · 2021Pooled it
- Altered striatal long-term potentiation in the eIF4E-TG mouse model of autism spectrum disorder.iScience · 2026Article
- Graph theory identifies altered prefrontal microcircuit organization in Shank3 mice, a mouse Model of autism.Cell reports · 2026Article
- Complement contributes to hyperactive behavior in the 16p11.2 hemideletion mouse model.Brain, behavior, and immunity · 2026Article
- Evaluation of Lead exposure's link to autism-like behavior and Shank 3 gene expression in C57BL/6J mice.The Journal of veterinary medical science · 2026Article
- Shared Genetic Networks in Schizophrenia and Bipolar Disorder: Hippocampal Volume-Mediated Neurobiological Mechanisms.Schizophrenia bulletin · 2026Article
- Potential glutamatergic and GABAergic false neurotransmitters in models of excitation-inhibition imbalance.Scientific reports · 2026Article
- How copy number variations shape brain developmental disorders: Unraveling the synaptic puzzle.Psychiatry and clinical neurosciences · 2026Review
- Graph Theory Identifies Autistic Patterns in the Prefrontal Circuit of a Mouse Model of Autism.Research square · 2026Article
- Sphingolipids in Emotional Well-Being.Journal of neurochemistry · 2026Review
- A chromosome region linked to neurodevelopmental disorders influences locomotor behavior through sex-specific neural circuits.Nature communications · 2026Article
- SEZ6L2 Loss Disrupts Motor Coordination, Cognitive Function, and Synaptic Connectivity.bioRxiv : the preprint server for biology · 2026Article
- Cell-type specific global reprogramming of the transcriptome and epigenome in induced neurons with the 16p11.2 neuropsychiatric CNVs.European journal of human genetics : EJHG · 2025Article
- Disruption of Cell-Type-Specific Molecular Programs of Medium Spiny Neurons in Autism.bioRxiv : the preprint server for biology · 2025Article
- TAOK2 drives opposing cilia length deficits in 16p11.2 deletion and duplication carriers.Stem cell reports · 2025Article
- The 16p11.2 microdeletion influences how early-life microbiota perturbations affect hippocampal development and behavior throughout the lifespan.bioRxiv : the preprint server for biology · 2025Article
- Mice with 16p11.2 Deletion and Duplication Show Alterations in Biological Processes Associated with White Matter.International journal of molecular sciences · 2025Article
- Long-term, cell type-specific effects of prenatal stress on dorsal striatum and relevant behaviors in mice.bioRxiv : the preprint server for biology · 2024Article
- Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.iScience · 2024Article
95 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
23 authors at 6 institutions in 2 countries.
Funding
Abstract
A deletion on human chromosome 16p11.2 is associated with autism spectrum disorders. We deleted the syntenic region on mouse chromosome 7F3. MRI and high-throughput single-cell transcriptomics revealed anatomical and cellular abnormalities, particularly in cortex and striatum of juvenile mutant mice (16p11(+/-)). We found elevated numbers of striatal medium spiny neurons (MSNs) expressing the dopamine D2 receptor (Drd2(+)) and fewer dopamine-sensitive (Drd1(+)) neurons in deep layers of cortex. Electrophysiological recordings of Drd2(+) MSN revealed synaptic defects, suggesting abnormal basal ganglia circuitry function in 16p11(+/-) mice. This is further supported by behavioral experiments showing hyperactivity, circling, and deficits in movement control. Strikingly, 16p11(+/-) mice showed a complete lack of habituation reminiscent of what is observed in some autistic individuals. Our findings unveil a fundamental role of genes affected by the 16p11.2 deletion in establishing the basal ganglia circuitry and provide insights in the pathophysiology of autism.
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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.