ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Loss of predominant Shank3 isoforms results in hippocampus-dependent impairments in behavior and synaptic transmission.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
189 citing papers in PubMed, 299 citations in OpenAlex.
- A randomized controlled trial into the effects of probiotics on electroencephalography in preschoolers with autism.Autism : the international journal of research and practice · 2023Trial
- Shank3 as a potential biomarker of antidepressant response to ketamine and its neural correlates in bipolar depression.Journal of affective disorders · 2015Trial
- Glycine-modulating Slc6a20a-ASO restores NMDA receptor function in SHANK2 and SHANK3-mutant mice and cortical organoids.Nature communications · 2026Article
- Potential glutamatergic and GABAergic false neurotransmitters in models of excitation-inhibition imbalance.Scientific reports · 2026Article
- Shank3 related oligodendrocyte alterations in autism are restored by Erk pathway inhibition.Molecular psychiatry · 2026Article
- Early-life sleep disruption in Shank3-deficient rats: A preclinical model for autism-related sleep mechanisms and interventions.Translational psychiatry · 2026Article
- Altered Structural Plasticity Mediated by mGlu and NMDA Receptors and Impaired Cognition in a Genetic ASD Model (Shank3The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- ATRX function beyond hippocampal CA1 is required for cognitive deficits in mouse models of intellectual disability.PloS one · 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
- 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
- Learning-Associated Flexibility of Cortical Taste Coding Is Impaired in Shank3 Knockout Mice.bioRxiv : the preprint server for biology · 2025Article
- Autism-like phenotype across the lifespan of Shank3B-mutant mice of both sexes.Journal of neurodevelopmental disorders · 2025Article
- Early Postnatal Shank3 Downregulation in the Nucleus Accumbens Impairs Performance in Social Conditioning Paradigms in Male Mice.The European journal of neuroscience · 2025Article
- Shank3 modulates Rpl3 expression and protein synthesis via mGlu5: implications for Phelan McDermid syndrome.Molecular psychiatry · 2025Article
- Animal models of autism spectrum disorder: Insights into genetic, structural and environmental models.Veterinarni medicina · 2025Review
- Atypical Cadherin FAT2 Is Required for Synaptic Integrity and Motor Behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Development of a brain-penetrant G9a methylase inhibitor to target Alzheimer's disease-associated proteopathology.Nature communications · 2025Article
- Altered Neural Activity in the Mesoaccumbens Pathway Underlies Impaired Social Reward Processing in Shank3-Deficient Rats.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Missense mutation in the activation segment of the kinase CK2 models Okur-Chung neurodevelopmental disorder and alters the hippocampal glutamatergic synapse.Molecular psychiatry · 2025Article
- Deciphering the Role of Shank3 in Dendritic Morphology and Synaptic Function Across Postnatal Developmental Stages in the Shank3B KO Mouse.Neuroscience bulletin · 2025Article
129 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
The Shank3 gene encodes a scaffolding protein that anchors multiple elements of the postsynaptic density at the synapse. Previous attempts to delete the Shank3 gene have not resulted in a complete loss of the predominant naturally occurring Shank3 isoforms. We have now characterized a homozygous Shank3 mutation in mice that deletes exon 21, including the Homer binding domain. In the homozygous state, deletion of exon 21 results in loss of the major naturally occurring Shank3 protein bands detected by C-terminal and N-terminal antibodies, allowing us to more definitively examine the role of Shank3 in synaptic function and behavior. This loss of Shank3 leads to an increased localization of mGluR5 to both synaptosome and postsynaptic density-enriched fractions in the hippocampus. These mice exhibit a decrease in NMDA/AMPA excitatory postsynaptic current ratio in area CA1 of the hippocampus, reduced long-term potentiation in area CA1, and deficits in hippocampus-dependent spatial learning and memory. In addition, these mice also exhibit motor-coordination deficits, hypersensitivity to heat, novelty avoidance, altered locomotor response to novelty, and minimal social abnormalities. These data suggest that Shank3 isoforms are required for normal synaptic transmission/plasticity in the hippocampus, as well as hippocampus-dependent spatial learning and memory.
Indexed as
Identifiers
What OpenQuestion holds
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.