ArticleTranslational psychiatry2018
Brain region-specific disruption of Shank3 in mice reveals a dissociation for cortical and striatal circuits in autism-related behaviors.
Article in Translational psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 121 citations in OpenAlex.
- Increased activity of DRD1-MSNs in dorsolateral striatum underlies Cry1Δ11 mutation-induced repetitive behaviors.Translational psychiatry · 2026Article
- Subcortical Dendritic Scaffolding in Autism Spectrum Disorder: A Testable ANK2-SCN2A-SHANK Framework.International journal of molecular sciences · 2026Review
- Social Novelty Recruits a Dysfunctional Nucleus Accumbens Ensemble That Drives Social Avoidance in abioRxiv : the preprint server for biology · 2026Article
- FOXG1 Hierarchically Shapes Synaptic Functions in Striatal iSPNs and Contributes to ASD Etiology.Neuroscience bulletin · 2026Article
- Cerebellar purkinje cell dysfunction contributes to gait impairments in Shank3-mutant mice.Molecular autism · 2026Article
- GABAFrontiers in pharmacology · 2026Review
- Shank3 establishes AMPA receptor subunit composition at cerebellar mossy fiber-granule cell synapses and is associated with altered regional microglial morphology.Neurobiology of disease · 2025Article
- Heightened empathic responses led by imbalanced cortico-amygdala circuit inbioRxiv : the preprint server for biology · 2025Article
- Deficiency of Shank3 in the nucleus accumbens reveals a loss of social-specific motivation.Communications biology · 2025Article
- Activity Deprivation Modulates the Shank3/Homer1/mGluR5 Signaling Pathway to Enable Synaptic Upscaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Early postnatal dysfunction of ACC PV interneurons in Shank3BMolecular psychiatry · 2025Article
- Article
- Developmental Disturbances in Animal Models of Autism Spectrum Disorder.Developmental neurobiology · 2025Review
- Reduced Neurite Arborization in Primary Dopaminergic Neurons in Autism-Like Shank3B-Deficient Mice.Molecular neurobiology · 2025Article
- Autism-like atypical face processing inScience advances · 2025Article
- Molecular Pathways, Neural Circuits and Emerging Therapies for Self-Injurious Behaviour.International journal of molecular sciences · 2025Review
- Late development of OCD-like phenotypes in Dlgap1 knockout mice.Psychopharmacology · 2025Article
- Behavioral decline in Shank3Molecular autism · 2024Article
- Automated Video Tracking of Autistic Children's Movement During Caregiver-Child Interaction: An Exploratory Study.Journal of autism and developmental disorders · 2024Article
- Assessing sociability using the Three-Chamber Social Interaction Test and the Reciprocal Interaction Test in a genetic mouse model of ASD.Behavioral and brain functions : BBF · 2024Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 1 institution in 1 country.
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Abstract
We previously reported a new line of Shank3 mutant mice which led to a complete loss of Shank3 by deleting exons 4-22 (Δe4-22) globally. Δe4-22 mice display robust ASD-like behaviors including impaired social interaction and communication, increased stereotypical behavior and excessive grooming, and a profound deficit in instrumental learning. However, the anatomical and neural circuitry underlying these behaviors are unknown. We generated mice with Shank3 selectively deleted in forebrain, striatum, and striatal D1 and D2 cells. These mice were used to interrogate the circuit/brain-region and cell-type specific role of Shank3 in the expression of autism-related behaviors. Whole-cell patch recording and biochemical analyses were used to study the synaptic function and molecular changes in specific brain regions. We found perseverative exploratory behaviors in mice with deletion of Shank3 in striatal inhibitory neurons. Conversely, self-grooming induced lesions were observed in mice with deletion of Shank3 in excitatory neurons of forebrain. However, social, communicative, and instrumental learning behaviors were largely unaffected in these mice, unlike what is seen in global Δe4-22 mice. We discovered unique patterns of change for the biochemical and electrophysiological findings in respective brain regions that reflect the complex nature of transcriptional regulation of Shank3. Reductions in Homer1b/c and membrane hyper-excitability were observed in striatal loss of Shank3. By comparison, Shank3 deletion in hippocampal neurons resulted in increased NMDAR-currents and GluN2B-containing NMDARs. These results together suggest that Shank3 may differentially regulate neural circuits that control behavior. Our study supports a dissociation of Shank3 functions in cortical and striatal neurons in ASD-related behaviors, and it illustrates the complexity of neural circuit mechanisms underlying these behaviors.
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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.