ReviewFrontiers in cellular neuroscience2014
Impaired activity-dependent neural circuit assembly and refinement in autism spectrum disorder genetic models.
Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 88 citations in OpenAlex.
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- Glia-to-glia serotonin signaling directs MMP-dependent infiltration for experience-dependent synapse pruning.PLoS biology · 2025Article
- Hippocampal-prefrontal functional neural networks in a rat model of fragile X syndrome are poorly organized with limited resiliency.Scientific reports · 2025Article
- Neurofibromin Deficiency Alters the Patterning and Prioritization of Motor Behaviors in a State-Dependent Manner.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- FMR1 genetically interacts with DISC1 to regulate glutamatergic synaptogenesis.Schizophrenia (Heidelberg, Germany) · 2024Article
- Neurofibromin deficiency alters the patterning and prioritization of motor behaviors in a state-dependent manner.bioRxiv : the preprint server for biology · 2024Article
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- A developmental neurotoxicity adverse outcome pathway (DNT-AOP) with voltage gate sodium channel (VGSC) inhibition as a molecular initiating event (MiE).EFSA journal. European Food Safety Authority · 2024Article
- Circuit-based intervention corrects excessive dentate gyrus output in the fragile X mouse model.eLife · 2024Article
- Characterization of NaLife science alliance · 2024Article
- Neurogenetics of Brain Connectivity: Current Approaches to the Study (Review).Sovremennye tekhnologii v meditsine · 2024Review
- Circuit-based intervention corrects excessive dentate gyrus output in the Fragile X mouse model.bioRxiv : the preprint server for biology · 2023Article
- Mechanisms Driving the Emergence of Neuronal Hyperexcitability in Fragile X Syndrome.International journal of molecular sciences · 2022Review
- Coexpression network architecture reveals the brain-wide and multiregional basis of disease susceptibility.Nature neuroscience · 2021Article
- Secreted C-type lectin regulation of neuromuscular junction synaptic vesicle dynamics modulates coordinated movement.Journal of cell science · 2021Article
- Autism Spectrum Disorders: Multiple Routes to, and Multiple Consequences of, Abnormal Synaptic Function and Connectivity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2021Review
- Synaptic Plasticity Induced by Differential Manipulation of Tonic and Phasic Motoneurons inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Novel Insights into the Role of UBE3A in Regulating Apoptosis and Proliferation.Journal of clinical medicine · 2020Article
- Synaptic Properties and Plasticity Mechanisms of Invertebrate Tonic and Phasic Neurons.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Early-use activity during circuit-specific critical periods refines brain circuitry by the coupled processes of eliminating inappropriate synapses and strengthening maintained synapses. We theorize these activity-dependent (A-D) developmental processes are specifically impaired in autism spectrum disorders (ASDs). ASD genetic models in both mouse and Drosophila have pioneered our insights into normal A-D neural circuit assembly and consolidation, and how these developmental mechanisms go awry in specific genetic conditions. The monogenic fragile X syndrome (FXS), a common cause of heritable ASD and intellectual disability, has been particularly well linked to defects in A-D critical period processes. The fragile X mental retardation protein (FMRP) is positively activity-regulated in expression and function, in turn regulates excitability and activity in a negative feedback loop, and appears to be required for the A-D remodeling of synaptic connectivity during early-use critical periods. The Drosophila FXS model has been shown to functionally conserve the roles of human FMRP in synaptogenesis, and has been centrally important in generating our current mechanistic understanding of the FXS disease state. Recent advances in Drosophila optogenetics, transgenic calcium reporters, highly-targeted transgenic drivers for individually-identified neurons, and a vastly improved connectome of the brain are now being combined to provide unparalleled opportunities to both manipulate and monitor A-D processes during critical period brain development in defined neural circuits. The field is now poised to exploit this new Drosophila transgenic toolbox for the systematic dissection of A-D mechanisms in normal versus ASD brain development, particularly utilizing the well-established Drosophila FXS disease model.
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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.