ArticleThe European journal of neuroscience2015
Shank1 regulates excitatory synaptic transmission in mouse hippocampal parvalbumin-expressing inhibitory interneurons.
Article in The European journal of neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- Sensory abnormalities in autism spectrum disorder and their in vitro modeling.Translational psychiatry · 2025Review
- Predicting cellular adaptation proteins dependent on eIF2α regulation under stress conditions: Physiological and pathophysiological implications in neuronal function.Computational and structural biotechnology journal · 2025Article
- A comprehensive review of GABA in autism spectrum disorders: associations, mechanisms, and therapeutic implications.Frontiers in psychiatry · 2025Review
- Mechanisms of glutamate receptors hypofunction dependent synaptic transmission impairment in the hippocampus of schizophrenia susceptibility gene Opcml-deficient mouse model.Molecular brain · 2024Article
- Overexpression of the schizophrenia risk gene C4 in PV cells drives sex-dependent behavioral deficits and circuit dysfunction.iScience · 2024Article
- Overexpression of the schizophrenia risk gene C4 in PV cells drives sex-dependent behavioral deficits and circuit dysfunction.bioRxiv : the preprint server for biology · 2024Article
- Spatially Resolved Transcriptomic Signatures of Hippocampal Subregions andbioRxiv : the preprint server for biology · 2024Article
- Spatially resolved transcriptomic signatures of hippocampal subregions andFrontiers in molecular neuroscience · 2024Article
- Roles of AMPA receptors in social behaviors.Frontiers in synaptic neuroscience · 2024Review
- Shank3 deletion in PV neurons is associated with abnormal behaviors and neuronal functions that are rescued by increasing GABAergic signaling.Molecular autism · 2023Article
- YBX1-Mediated DNA Methylation-Dependent SHANK3 Expression in PBMCs and Developing Cortical Interneurons in Schizophrenia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Behavioral and Sensory Deficits Associated with Dysfunction of GABAergic System in a NovelInternational journal of molecular sciences · 2023Article
- Genetic impairment of folate metabolism regulates cortical interneurons and social behavior.Frontiers in neuroscience · 2023Article
- Continuous high-frequency deep brain stimulation of the anterior insula modulates autism-like behavior in a valproic acid-induced rat model.Journal of translational medicine · 2022Article
- Chronic stress causes striatal disinhibition mediated by SOM-interneurons in male mice.Nature communications · 2022Article
- Neurobiology of ARID1B haploinsufficiency related to neurodevelopmental and psychiatric disorders.Molecular psychiatry · 2022Review
- Excitatory and Inhibitory Synaptic Imbalance Caused by Brain-Derived Neurotrophic Factor Deficits During Development in a Valproic Acid Mouse Model of Autism.Frontiers in molecular neuroscience · 2022Article
- Cortical interneurons in autism.Nature neuroscience · 2021Review
- Comparison of SHANK3 deficiency in animal models: phenotypes, treatment strategies, and translational implications.Journal of neurodevelopmental disorders · 2021Review
- Truncating variants in the SHANK1 gene are associated with a spectrum of neurodevelopmental disorders.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The Shank genes (SHANK1, 2, 3) encode scaffold proteins highly enriched in postsynaptic densities where they regulate synaptic structure in spiny neurons. Mutations in human Shank genes are linked to autism spectrum disorder and schizophrenia. Shank1 mutant mice exhibit intriguing cognitive phenotypes reminiscent of individuals with autism spectrum disorder. However, the molecular mechanisms leading to the human pathophysiological phenotypes and mouse behaviors have not been elucidated. In this study it is shown that Shank1 protein is highly localized in parvalbumin-expressing (PV+) fast-spiking inhibitory interneurons in the hippocampus. Importantly, a lack of Shank1 in hippocampal CA1 PV+ neurons reduced excitatory synaptic inputs and inhibitory synaptic outputs to pyramidal neurons. Furthermore, it is demonstrated that hippocampal CA1 pyramidal neurons in Shank1 mutant mice exhibit a shift in the excitatory and inhibitory balance (E-I balance), a pathophysiological hallmark of autism spectrum disorder. The mutant mice also exhibit lower expression of gephyrin (a scaffold component of inhibitory synapses), supporting the dysregulation of E-I balance in the hippocampus. These results suggest that Shank1 scaffold in PV+ interneurons regulates excitatory synaptic strength and participates in the maintenance of E-I balance in excitatory neurons.
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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.