ArticleBiological psychiatry2019
Early Correction of N-Methyl-D-Aspartate Receptor Function Improves Autistic-like Social Behaviors in Adult Shank2
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Article in Biological psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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44citing papers in PubMed, 1 pooled it
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- NMDA antagonist agents for the treatment of symptoms in autism spectrum disorder: a systematic review and meta-analysis.Frontiers in pharmacology · 2024Pooled it
- Autism-like phenotypes and increased NMDAR2D expression in mice with KDM5B histone lysine demethylase deficiency.Science advances · 2026Article
- Article
- Social memory engram formation impairment in neuroligin-3 R451C knock-in mice is caused by disrupted prefrontal NMDA receptor-dependent potentiation.Communications biology · 2025Article
- Protein-truncating variants and deletions of SHANK2 are associated with autism spectrum disorder and other neurodevelopmental concerns.Journal of neurodevelopmental disorders · 2025Article
- Identification of biomarkers related to propionate metabolism in schizophrenia.Frontiers in psychiatry · 2025Article
- A comparative view of human and mouse telencephalon inhibitory neuron development.Development (Cambridge, England) · 2025Review
- The Use of Nutraceutical and Pharmacological Strategies in Murine Models of Autism Spectrum Disorder.Cells · 2024Review
- Differential effectiveness of dietary zinc supplementation with autism-related behaviours inPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Article
- Remodeling of the postsynaptic proteome in male mice and marmosets during synapse development.Nature communications · 2024Article
- Porphyrinuria in Autism Spectrum Disorder: A Review.Current medicinal chemistry · 2024Review
- Shank2 identifies a subset of glycinergic neurons involved in altered nociception in an autism model.Molecular autism · 2023Article
- Downregulation of the Autism Spectrum Disorder GeneJBMR plus · 2023Article
- Autism Spectrum Disorder: Neurodevelopmental Risk Factors, Biological Mechanism, and Precision Therapy.International journal of molecular sciences · 2023Review
- The Role of Zinc and NMDA Receptors in Autism Spectrum Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Enhanced fear limits behavioral flexibility in Shank2-deficient mice.Molecular autism · 2022Article
- A Mini-Review Regarding the Modalities to Study Neurodevelopmental Disorders-Like Impairments in Zebrafish-Focussing on Neurobehavioural and Psychological Responses.Brain sciences · 2022Review
- Modelling Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD) Using Mice and Zebrafish.International journal of molecular sciences · 2022Review
- Age, brain region, and gene dosage-differential transcriptomic changes inFrontiers in molecular neuroscience · 2022Article
- A Deficiency of the Psychiatric Risk Gene DLG2/PSD-93 Causes Excitatory Synaptic Deficits in the Dorsolateral Striatum.Frontiers in molecular neuroscience · 2022Article
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Authors and funding
30 authors at 9 institutions in 3 countries.
Changuk ChungDepartment of Biological Sciences, South Korea; Center for Synaptic Brain Dysfunctions, Institute for Basic Science, South Korea.
Seungmin HaDepartment of Biological Sciences, South Korea.
Hyojin KangDepartment of Convergence Technology Research, Korea Institute of Science and Technology Information, Daejeon, South Korea.
Jiseok LeeCenter for Synaptic Brain Dysfunctions, Institute for Basic Science, South Korea.
Seung Min UmDepartment of Biological Sciences, South Korea.
Haidun YanDepartment of Pediatrics, Duke University, Durham, North Carolina.
Ye-Eun YooDepartment of Biological Sciences, South Korea.
Taesun YooDepartment of Biological Sciences, South Korea.
Hwajin JungCenter for Synaptic Brain Dysfunctions, Institute for Basic Science, South Korea.
Dongwon LeeCenter for Synaptic Brain Dysfunctions, Institute for Basic Science, South Korea.
Eunee LeeCenter for Synaptic Brain Dysfunctions, Institute for Basic Science, South Korea.
Seungjoon LeeDepartment of Biological Sciences, South Korea.
Jihye KimCenter for Synaptic Brain Dysfunctions, Institute for Basic Science, South Korea.
Ryunhee KimDepartment of Biological Sciences, South Korea.
Yonghan KwonDepartment of Biological Sciences, South Korea.
Woohyun KimDepartment of Biological Sciences, South Korea.
Hyosang KimDepartment of Biological Sciences, South Korea.
Lara DuffneyDepartment of Pediatrics, Duke University, Durham, North Carolina.
Doyoun KimCenter for Synaptic Brain Dysfunctions, Institute for Basic Science, South Korea.
Won MahDepartment of Anatomy and Neurobiology, School of Dentistry, Kyungpook National University, Daegu, South Korea.
Hyejung WonDepartment of Neurology, Center for Autism Research and Treatment, Semel Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.
Seojung MoDepartment of Anatomy and Division of Brain Korea 21, Biomedical Science, College of Medicine, Korea University, Seoul, South Korea.
Jin Yong KimDepartment of Anatomy and Division of Brain Korea 21, Biomedical Science, College of Medicine, Korea University, Seoul, South Korea.
Chae-Seok LimSchool of Biological Sciences, Seoul National University, Seoul, South Korea.
Bong-Kiun KaangSchool of Biological Sciences, Seoul National University, Seoul, South Korea.
Tobias M BoeckersInstitute for Anatomy and Cell Biology, Ulm University, Ulm, Germany.
Yeonseung ChungDepartment of Mathematical Sciences, Korea Advanced Institute for Science and Technology, South Korea.
Hyun KimDepartment of Anatomy and Division of Brain Korea 21, Biomedical Science, College of Medicine, Korea University, Seoul, South Korea.
Yong-Hui JiangDepartment of Pediatrics, Duke University, Durham, North Carolina; Department of Neurobiology, Duke University, Durham, North Carolina; Cell and Molecular Biology Program, Duke University, Durham, North Carolina; Duke Institute of Brain Science, Duke University, Durham, North Carolina; Genomics and Genetics Program, Duke University, Durham, North Carolina.
Eunjoon KimDepartment of Biological Sciences, South Korea; Center for Synaptic Brain Dysfunctions, Institute for Basic Science, South Korea. Electronic address: kime@kaist.ac.kr.
Institute for Basic Science · KRKorea University · KRDuke University · USSeoul National University · KRKorea Institute of Science & Technology Information · KRKyungpook National University · KRNational Institute for Mathematical Sciences · KRUniversität Ulm · DEUniversity of California, Los Angeles · US
Funding
Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9MMolecular and circuitry mechanism underlying autism behaviors in Shank3 mouse modelsR01MH117289 · NIMH · YALE UNIVERSITY · PI JIANG, YONG-HUI · 2019 to 2023
$3.2MCharacterizing the (epi)genetics of oxytocin response in clinical and animal modelsR01HD088007 · NICHD · DUKE UNIVERSITY · PI GREGORY, SIMON G, JIANG, YONG-HUI · 2017 to 2021
$2.9MEpigenetic Therapy and Prader-Willi SyndromeR01HD088626 · NICHD · YALE UNIVERSITY · PI JIANG, YONG-HUI, JIN, JIAN · 2017 to 2021
$2.8MAnalysis of Shank3 Complete and Temporal and Spatial Specific Knockout MiceR01MH098114 · NIMH · DUKE UNIVERSITY · PI JIANG, YONG-HUI · 2012 to 2016
$2.2MConnecting gene regulatory mechanisms in human brain to psychiatric illnessR00MH113823 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WON, HYEJUNG · 2018 to 2020
$719kA novel neural circuit analysis paradigm to model autism in miceR21MH104316 · NIMH · DUKE UNIVERSITY · PI JIANG, YONG-HUI · 2014 to 2015
$435kA novel paradigm to dissect the function connectivity in Shank3 autism modelR21HD087795 · NICHD · YALE UNIVERSITY · PI JIANG, YONG-HUI · 2017 to 2018
$434kTherapeutic potential for Prader-Willi syndromeR21HD077197 · NICHD · DUKE UNIVERSITY · PI JIANG, YONG-HUI · 2014 to 2015
$413kNCATS NIH HHS UL1 TR001863NICHD NIH HHS R01 HD088007NICHD NIH HHS R01 HD088626NICHD NIH HHS R21 HD077197NICHD NIH HHS R21 HD087795NIMH NIH HHS R00 MH113823NIMH NIH HHS R01 MH098114NIMH NIH HHS R01 MH117289NIMH NIH HHS R21 MH104316
Abstract
backgroundAutism spectrum disorder involves neurodevelopmental dysregulations that lead to visible symptoms at early stages of life. Many autism spectrum disorder-related mechanisms suggested by animal studies are supported by demonstrated improvement in autistic-like phenotypes in adult animals following experimental reversal of dysregulated mechanisms. However, whether such mechanisms also act at earlier stages to cause autistic-like phenotypes is unclear.
methodsWe used Shank2
resultsEarly correction of a dysregulated mechanism in young mice prevents manifestation of autistic-like social behaviors in adult mice. Shank2
conclusionsEarly NMDAR hyperfunction leads to late NMDAR hypofunction and autistic-like social behaviors in Shank2
Indexed as
Social BehaviorAge FactorsAnimalsAutism Spectrum DisorderBehavior, AnimalDisease Models, AnimalExcitatory Amino Acid AntagonistsMemantineMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsReceptors, N-Methyl-D-AspartateExcitatory Amino Acid AntagonistsMemantineNerve Tissue ProteinsReceptors, N-Methyl-D-AspartateShank2 protein, mouseAutismMemantineNMDA receptorSHANK2SynapseTreatment
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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.