ArticleNature neuroscience2016
SHANK3 controls maturation of social reward circuits in the VTA.
Article in Nature neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.
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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
104 citing papers in PubMed, 1 synthesis or guideline pooled it, 168 citations in OpenAlex.
- A Systematic Review of Brainstem Contributions to Autism Spectrum Disorder.Frontiers in integrative neuroscience · 2021Pooled it
- Social Novelty Recruits a Dysfunctional Nucleus Accumbens Ensemble That Drives Social Avoidance in abioRxiv : the preprint server for biology · 2026Article
- Article
- A homecage operant paradigm reveals behavioral dynamics of social motivation in mice.Cell reports methods · 2026Article
- Review
- Prenatal valproate exposure alters midbrain and striatal neuronal morphology along with dopamine levels.Brain structure & function · 2026Article
- Reduced volume of neuromodulatory brainstem nuclei is associated with early hallucination-related vulnerability in Parkinson's disease.Brain communications · 2026Article
- 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
- Deficiency of Shank3 in the nucleus accumbens reveals a loss of social-specific motivation.Communications biology · 2025Article
- The emergence of electrical activity in human brain organoids.Stem cell reports · 2025Review
- Potentiation of Nigra-Striatal Dopaminergic Projection Underpins Core Autism-Like Behaviors in Valproate-Exposed Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- How dopamine guides our social world.Pharmacological reviews · 2025Review
- Early Postnatal Shank3 Downregulation in the Nucleus Accumbens Impairs Performance in Social Conditioning Paradigms in Male Mice.The European journal of neuroscience · 2025Article
- Article
- Altered Neural Activity in the Mesoaccumbens Pathway Underlies Impaired Social Reward Processing in Shank3-Deficient Rats.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Reduced Neurite Arborization in Primary Dopaminergic Neurons in Autism-Like Shank3B-Deficient Mice.Molecular neurobiology · 2025Article
- VTA µ-Opioidergic Neurons Facilitate Low Sociability in Protracted Opioid Abstinence.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Deciphering the Role of Shank3 in Dendritic Morphology and Synaptic Function Across Postnatal Developmental Stages in the Shank3B KO Mouse.Neuroscience bulletin · 2025Article
- Review: Dopamine, Serotonin, and the Translational Neuroscience of Aggression in Autism Spectrum Disorder.JAACAP open · 2025Review
- Synaptotagmin-11 deficiency mediates schizophrenia-like behaviors in mice via dopamine over-transmission.Nature communications · 2024Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Haploinsufficiency of SHANK3, encoding the synapse scaffolding protein SHANK3, leads to a highly penetrant form of autism spectrum disorder. How SHANK3 insufficiency affects specific neural circuits and how this is related to specific symptoms remains elusive. Here we used shRNA to model Shank3 insufficiency in the ventral tegmental area of mice. We identified dopamine (DA) and GABA cell-type-specific changes in excitatory synapse transmission that converge to reduce DA neuron activity and generate behavioral deficits, including impaired social preference. Administration of a positive allosteric modulator of the type 1 metabotropic glutamate receptors mGluR1 during the first postnatal week restored DA neuron excitatory synapse transmission and partially rescued the social preference defects, while optogenetic DA neuron stimulation was sufficient to enhance social preference. Collectively, these data reveal the contribution of impaired ventral tegmental area function to social behaviors and identify mGluR1 modulation during postnatal development as a potential treatment strategy.
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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.