ArticleMolecular psychiatry2022
Inhibition of Trpv4 rescues circuit and social deficits unmasked by acute inflammatory response in a Shank3 mouse model of Autism.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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
29 citing papers in PubMed, 43 citations in OpenAlex.
- Disruption of FOXG1 Impairs the Development of Striatal dSPNs, Thereby Contributing to ASD-Like Phenotypes.Neuroscience bulletin · 2026Article
- Inflammation increases the penetrance of behavioral impairment in Shank3 haploinsufficiency mice - can it explain the behavioral regression in Autism?Molecular psychiatry · 2026Article
- Acetaminophen-induced liver injury triggers short- and long-term neuroinflammation, blood-brain barrier disruption, and behavioral deficits in a genetic mouse model of autism.Acta neuropathologica communications · 2026Article
- Social Novelty Recruits a Dysfunctional Nucleus Accumbens Ensemble That Drives Social Avoidance in abioRxiv : the preprint server for biology · 2026Article
- Review
- Microglial Lyn Kinase-TRPV4 axis mediates social deficits in a maternal immune activation model.Journal of neuroinflammation · 2026Article
- A Drd1-cre mouse line with nucleus accumbens gene dysregulation exhibits blunted fentanyl seeking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Transient Receptor Potential Channels as Key Regulators of Neuroinflammation in Neurological Disorders: Mechanistic Insights, Therapeutic Potentials, and Future Directions.CNS neuroscience & therapeutics · 2025Review
- Deficiency of Shank3 in the nucleus accumbens reveals a loss of social-specific motivation.Communications biology · 2025Article
- Inflammation increases the penetrance of behavioral impairment inbioRxiv : the preprint server for biology · 2025Article
- Article
- Early Postnatal Shank3 Downregulation in the Nucleus Accumbens Impairs Performance in Social Conditioning Paradigms in Male Mice.The European journal of neuroscience · 2025Article
- Metalomics Revealed that Changes of Serum Elements were Associated with Oxidative Stress-Induced Inflammation of Cortex in a Mouse Model of Autism.Biological trace element research · 2025Article
- Translational research approach to social orienting deficits in autism: the role of superior colliculus-ventral tegmental pathway.Molecular psychiatry · 2025Article
- Primary sensory neuron dysfunction underlying mechanical itch hypersensitivity in a Shank3 mouse model of autism.Translational psychiatry · 2025Article
- Gut microbiota and brain-resident CD4Nature communications · 2025Article
- TRPV4 Channel in Neurological Disease: from Molecular Mechanisms to Therapeutic Potential.Molecular neurobiology · 2025Review
- Article
- Evidence for common mechanisms of pathology between SHANK3 and other genes of Phelan-McDermid syndrome.Clinical genetics · 2024Review
- The PFC-LH-VTA pathway contributes to social deficits in IRSp53-mutant mice.Molecular psychiatry · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the SHANK3 gene have been recognized as a genetic risk factor for Autism Spectrum Disorder (ASD), a neurodevelopmental disease characterized by social deficits and repetitive behaviors. While heterozygous SHANK3 mutations are usually the types of mutations associated with idiopathic autism in patients, heterozygous deletion of Shank3 gene in mice does not commonly induce ASD-related behavioral deficit. Here, we used in-vivo and ex-vivo approaches to demonstrate that region-specific neonatal downregulation of Shank3 in the Nucleus Accumbens promotes D1R-medium spiny neurons (D1R-MSNs) hyperexcitability and upregulates Transient Receptor Potential Vanilloid 4 (Trpv4) to impair social behavior. Interestingly, genetically vulnerable Shank3
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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.