ArticleNature medicine2017
Thalamic miR-338-3p mediates auditory thalamocortical disruption and its late onset in models of 22q11.2 microdeletion.
Article in Nature medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
- Striatal dopaminergic function and cortical functional connectivity in 22q11.2 deletion syndrome: an integrative multimodalMolecular psychiatry · 2026Article
- Auditory and Visual Thalamocortical Connectivity Alterations in Unmedicated People With Schizophrenia: An Individualized Sensory Thalamic Localization and Resting-State Functional Connectivity Study.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2025Article
- Nucleus Reuniens-Elicited Delta Oscillations Disable the Prefrontal Cortex in Schizophrenia.Cells · 2025Review
- Candidate Key Proteins of Tinnitus in the Auditory and Motor Systems of the Thalamus.International journal of molecular sciences · 2025Article
- Circ_DLG1 facilitates cell proliferation and metastasis of esophageal squamous cell carcinoma via upregulating MAP3K9.Esophagus : official journal of the Japan Esophageal Society · 2025Article
- Fine Regulation of MicroRNAs in Gene Regulatory Networks and Pathophysiology.International journal of molecular sciences · 2025Review
- The acoustic startle response in 22q11 deletion syndrome: from animal models to humans.Frontiers in neuroscience · 2025Review
- Auditory and Visual Thalamocortical Connectivity Alterations in Unmedicated People with Schizophrenia: An Individualized Sensory Thalamic Localization and Resting-State Functional Connectivity Study.medRxiv : the preprint server for health sciences · 2024Article
- Next-generation sequencing profiling of miRNAs in individuals with 22q11.2 deletion syndrome revealed altered expression of miR-185-5p.Human genomics · 2024Article
- Effects of gene dosage and development on subcortical nuclei volumes in individuals with 22q11.2 copy number variations.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Longitudinal MicroRNA Signature of Conversion to Psychosis.Schizophrenia bulletin · 2024Article
- Longitudinal Development of Thalamocortical Functional Connectivity in 22q11.2 Deletion Syndrome.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2024Article
- Functional localization of the human auditory and visual thalamus using a thalamic localizer functional magnetic resonance imaging task.Imaging neuroscience (Cambridge, Mass.) · 2024Article
- Review: Genes Involved in Mitochondrial Physiology Within 22q11.2 Deleted Region and Their Relevance to Schizophrenia.Schizophrenia bulletin · 2023Article
- Effects of Gene Dosage and Development on Subcortical Nuclei Volumes in Individuals with 22q11.2 Copy Number Variations.bioRxiv : the preprint server for biology · 2023Article
- Serum microRNAs associated with concussion in football players.Frontiers in neurology · 2023Article
- MicroRNA 3' ends shorten during adolescent brain maturation.Frontiers in molecular neuroscience · 2023Article
- Article
- Schizophrenia Risk Mediated by microRNA Target Genes Overlapped by Genome-Wide Rare Copy Number Variation in 22q11.2 Deletion Syndrome.Frontiers in genetics · 2022Article
- Article
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12 authors at 1 institution in 1 country.
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Abstract
Although 22q11.2 deletion syndrome (22q11DS) is associated with early-life behavioral abnormalities, affected individuals are also at high risk for the development of schizophrenia symptoms, including psychosis, later in life. Auditory thalamocortical (TC) projections recently emerged as a neural circuit that is specifically disrupted in mouse models of 22q11DS (hereafter referred to as 22q11DS mice), in which haploinsufficiency of the microRNA (miRNA)-processing-factor-encoding gene Dgcr8 results in the elevation of the dopamine receptor Drd2 in the auditory thalamus, an abnormal sensitivity of thalamocortical projections to antipsychotics, and an abnormal acoustic-startle response. Here we show that these auditory TC phenotypes have a delayed onset in 22q11DS mice and are associated with an age-dependent reduction of miR-338-3p, a miRNA that targets Drd2 and is enriched in the thalamus of both humans and mice. Replenishing depleted miR-338-3p in mature 22q11DS mice rescued the TC abnormalities, and deletion of Mir338 (which encodes miR-338-3p) or reduction of miR-338-3p expression mimicked the TC and behavioral deficits and eliminated the age dependence of these deficits. Therefore, miR-338-3p depletion is necessary and sufficient to disrupt auditory TC signaling in 22q11DS mice, and it may mediate the pathogenic mechanism of 22q11DS-related psychosis and control its late onset.
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