ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
MHCI requires MEF2 transcription factors to negatively regulate synapse density during development and in disease.
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 48 papers.
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Who cites it
48 citing papers in PubMed, 92 citations in OpenAlex.
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- Glutamate Signaling and Neuroligin/Neurexin Adhesion Play Opposing Roles That Are Mediated by Major Histocompatibility Complex I Molecules in Cortical Synapse Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- An innate immune response to adeno-associated virus genomes decreases cortical dendritic complexity and disrupts synaptic transmission.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Contactomics of Microglia and Intercellular Communication.Advances in neurobiology · 2024Review
- Microglia Modulate Neurodevelopment in Autism Spectrum Disorder and Schizophrenia.International journal of molecular sciences · 2023Review
- Human brain organoid model of maternal immune activation identifies radial glia cells as selectively vulnerable.Molecular psychiatry · 2023Article
- The Role of MEF2 Transcription Factor Family in Neuronal Survival and Degeneration.International journal of molecular sciences · 2023Review
- Article
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- Neurological consequences of neurovascular unit and brain vasculature damages: potential risks for pregnancy infections and COVID-19-babies.The FEBS journal · 2022Review
- Homotypic and heterotypicCurrent research in immunology · 2022Review
- Interferon-γ exposure of human iPSC-derived neurons alters major histocompatibility complex I and synapsin protein expression.Frontiers in psychiatry · 2022Article
- Increased excitation-inhibition balance and loss of GABAergic synapses in the serine racemase knockout model of NMDA receptor hypofunction.Journal of neurophysiology · 2021Article
- New Insights Regarding Diagnosis and Medication for Schizophrenia Based on Neuronal Synapse-Microglia Interaction.Journal of personalized medicine · 2021Review
- Involvement of myocyte enhancer factor 2c in the pathogenesis of autism spectrum disorder.Heliyon · 2021Review
- Sequential perturbations to mouse corticogenesis following in utero maternal immune activation.eLife · 2021Article
- Prenatal stress effects on offspring brain and behavior: Mediators, alterations and dysregulated epigenetic mechanisms.Journal of biosciences · 2021Review
- Overexpression of astroglial major histocompatibility complex class I in the medial prefrontal cortex impairs visual discrimination learning in mice.Molecular brain · 2020Article
- Sex-specific impact of prenatal androgens on social brain default mode subsystems.Molecular psychiatry · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Major histocompatibility complex class I (MHCI) molecules negatively regulate cortical connections and are implicated in neurodevelopmental disorders, including autism spectrum disorders and schizophrenia. However, the mechanisms that mediate these effects are unknown. Here, we report a novel MHCI signaling pathway that requires the myocyte enhancer factor 2 (MEF2) transcription factors. In young rat cortical neurons, MHCI regulates MEF2 in an activity-dependent manner and requires calcineurin-mediated activation of MEF2 to limit synapse density. Manipulating MEF2 alone alters synaptic strength and GluA1 content, but not synapse density, implicating activity-dependent MEF2 activation as critical for MHCI signaling. The MHCI-MEF2 pathway identified here also mediates the effects of a mouse model of maternal immune activation (MIA) on connectivity in offspring. MHCI and MEF2 levels are higher, and synapse density is lower, on neurons from MIA offspring. Most important, dysregulation of MHCI and MEF2 is required for the MIA-induced reduction in neural connectivity. These results identify a previously unknown MHCI-calcineurin-MEF2 signaling pathway that regulates the establishment of cortical connections and mediates synaptic defects caused by MIA, a risk factor for autism spectrum disorders and schizophrenia.
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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.