ArticleNature neuroscience2016
Early hyperactivity and precocious maturation of corticostriatal circuits in Shank3B(-/-) mice.
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 149 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
149 citing papers in PubMed, 1 synthesis or guideline pooled it, 246 citations in OpenAlex.
- Genetic variability in scaffolding proteins and risk for schizophrenia and autism-spectrum disorders: a systematic review.Journal of psychiatry & neuroscience : JPN · 2018Pooled it
- Disruption of FOXG1 Impairs the Development of Striatal dSPNs, Thereby Contributing to ASD-Like Phenotypes.Neuroscience bulletin · 2026Article
- Altered striatal long-term potentiation in the eIF4E-TG mouse model of autism spectrum disorder.iScience · 2026Article
- Preserved social development but impaired executive function in aResearch square · 2026Article
- Indirect pathway neurons in the tail of the striatum regulate inhibitory control over sensory driven behavior.Science advances · 2026Article
- The role of ucOCN in aerobic exercise induced amelioration of autism spectrum disorder phenotypes.iScience · 2026Article
- Subcortical Dendritic Scaffolding in Autism Spectrum Disorder: A Testable ANK2-SCN2A-SHANK Framework.International journal of molecular sciences · 2026Review
- Npas4 regulates synaptic development in the patch/striosome compartment and early affective vocalization in neonatal mice.Molecular brain · 2026Article
- Disrupted Development of the mPFC-Thalamic Circuit in Shank3Molecular psychiatry · 2026Article
- Targeting synaptic plasticity and acetylcholine dysregulation in the medial prefrontal cortex: Rosmarinic acid attenuates Autism-like phenotypes in Shank3BPsychopharmacology · 2026Article
- Aberrant medial ganglionic eminence (MGE) GABAergic neurogenesis contributes to Huntington's disease pathogenesis.Neurobiology of disease · 2026Article
- Extracellular vesicles from stem cells rescue cellular phenotypes and behavioral deficits in SHANK3-associated ASD neuronal and mouse models.Cell death & disease · 2026Article
- Postnatal reduction of eIF4E overexpression in D1-SPNs ameliorates KCNQ channel dysfunction, hyperexcitability and ASD-like behaviours.Cellular and molecular life sciences : CMLS · 2026Article
- Sex- and etiology-specific effects on predictive processing in the inferior colliculus of two rat models of autism.Communications biology · 2026Article
- Disrupted cortex-wide dynamics impair motor planning in Shank3-mutant mice.bioRxiv : the preprint server for biology · 2026Article
- Early postnatal dysfunction of ACC PV interneurons in Shank3BMolecular psychiatry · 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
- Article
- Striatal output regulates the postnatal maturation of cortical circuits.Cell reports · 2025Article
- Shank3 modulates Rpl3 expression and protein synthesis via mGlu5: implications for Phelan McDermid syndrome.Molecular psychiatry · 2025Article
89 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
5 authors at 2 institutions in 1 country.
Funding
Abstract
Some autistic individuals exhibit abnormal development of the caudate nucleus and associative cortical areas, suggesting potential dysfunction of cortico-basal ganglia (BG) circuits. Using optogenetic and electrophysiological approaches in mice, we identified a narrow postnatal period that is characterized by extensive glutamatergic synaptogenesis in striatal spiny projection neurons (SPNs) and a concomitant increase in corticostriatal circuit activity. SPNs during early development have high intrinsic excitability and respond strongly to cortical afferents despite sparse excitatory inputs. As a result, striatum and corticostriatal connectivity are highly sensitive to acute and chronic changes in cortical activity, suggesting that early imbalances in cortical function alter BG development. Indeed, a mouse model of autism with deletions in Shank3 (Shank3B(-/-)) shows early cortical hyperactivity, which triggers increased SPN excitatory synapse and corticostriatal hyperconnectivity. These results indicate that there is a tight functional coupling between cortex and striatum during early postnatal development and suggest a potential common circuit dysfunction that is caused by cortical hyperactivity.
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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.