ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Reduced excitatory neurotransmission and mild autism-relevant phenotypes in adolescent Shank3 null mutant mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 238 papers, 2 of them syntheses that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
238 citing papers in PubMed, 2 syntheses or guidelines pooled it, 378 citations in OpenAlex.
- A systematic-review of olfactory deficits in neurodevelopmental disorders: From mouse to human.Neuroscience and biobehavioral reviews · 2021Pooled it
- Genetic variability in scaffolding proteins and risk for schizophrenia and autism-spectrum disorders: a systematic review.Journal of psychiatry & neuroscience : JPN · 2018Pooled it
- A randomized controlled trial of intranasal oxytocin in Phelan-McDermid syndrome.Molecular autism · 2021Trial
- Is there an effect of intranasal insulin on development and behaviour in Phelan-McDermid syndrome? A randomized, double-blind, placebo-controlled trial.European journal of human genetics : EJHG · 2016Trial
- Preserved social development but impaired executive function in aResearch square · 2026Article
- Aberrant Fear: Biological Underpinnings Relevant to Psychosis, Antipsychotic Drugs, and Psychotherapeutic Treatments, a Translational Approach.International journal of molecular sciences · 2026Review
- Genetic Rescue of Pathogenic O-GlcNAc Dyshomeostasis Associated with Microcephaly and Motor Deficits.eNeuro · 2026Article
- Article
- Dynamic recruitment of CaMKII into SHANK3 phase-separated condensates tunes postsynaptic density remodeling during long-term potentiation.Nature communications · 2026Article
- Chronic allergic lung inflammation is associated with brain mast cell-mediated suppression of neuronal activity and behavioral changes in mice.Respiratory research · 2026Article
- A neuron type-specific microexon in Ank3/ankyrin-G modulates calcium activity and neuronal excitability.Nature communications · 2026Article
- Early-life sleep disruption in Shank3-deficient rats: A preclinical model for autism-related sleep mechanisms and interventions.Translational psychiatry · 2026Article
- Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity.Frontiers in synaptic neuroscience · 2026Review
- A neuron type-specific microexon inbioRxiv : the preprint server for biology · 2025Article
- Deficiency of Shank3 in the nucleus accumbens reveals a loss of social-specific motivation.Communications biology · 2025Article
- A Frank Assessment of SHANK: Impacts of Pathogenic Variations in SHANK3 on Preclinical Models of Phelan McDermid Syndrome.Autism research : official journal of the International Society for Autism Research · 2025Review
- Autism-like phenotype across the lifespan of Shank3B-mutant mice of both sexes.Journal of neurodevelopmental disorders · 2025Article
- The retrotransposon-derived capsid genes PNMA1 and PNMA4 maintain reproductive capacity.Nature aging · 2025Article
- Altered Neural Activity in the Mesoaccumbens Pathway Underlies Impaired Social Reward Processing in Shank3-Deficient Rats.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Interleukin-6 produces behavioral deficits in pre-pubescent mice independent of neuroinflammation.Brain, behavior, and immunity · 2025Article
178 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 4 countries.
Funding
Abstract
Mutations in the synaptic scaffolding protein gene SHANK3 are strongly implicated in autism and Phelan-McDermid 22q13 deletion syndrome. The precise location of the mutation within the Shank3 gene is key to its phenotypic outcomes. Here, we report the physiological and behavioral consequences of null and heterozygous mutations in the ankyrin repeat domain in Shank3 mice. Both homozygous and heterozygous mice showed reduced glutamatergic transmission and long-term potentiation in the hippocampus with more severe deficits detected in the homozygous mice. Three independent cohorts were evaluated for magnitude and replicability of behavioral endophenotypes relevant to autism and Phelan-McDermid syndrome. Mild social impairments were detected, primarily in juveniles during reciprocal interactions, while all genotypes displayed normal adult sociability on the three-chambered task. Impaired novel object recognition and rotarod performance were consistent across cohorts of null mutants. Repetitive self-grooming, reduced ultrasonic vocalizations, and deficits in reversal of water maze learning were detected only in some cohorts, emphasizing the importance of replication analyses. These results demonstrate the exquisite specificity of deletions in discrete domains within the Shank3 gene in determining severity of symptoms.
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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.