ArticlePloS one2012
Neuroligin-1 loss is associated with reduced tenacity of excitatory synapses.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Single-Cell Transcriptomic Analysis of Macaque LGN Neurons Reveals Novel Subpopulations.Molecular neurobiology · 2026Article
- Revealing acute consequences of rapid degradation of synaptic fusion proteins at individual synapses using Auxin-Inducible Degron 2 technology.Communications biology · 2025Article
- How do we get from hyperexcitability to excitotoxicity in amyotrophic lateral sclerosis?Brain : a journal of neurology · 2024Review
- Linking spontaneous and stimulated spine dynamics.Communications biology · 2023Article
- Impaired AMPARs Translocation into Dendritic Spines with Motor Skill Learning in the Fragile X Mouse Model.eNeuro · 2023Article
- Neuroligin Plays a Role in Ethanol-Induced Disruption of Memory and Corresponding Modulation of Glutamate Receptor Expression.Frontiers in behavioral neuroscience · 2022Article
- Neuroligin-1 mediates presynaptic maturation through brain-derived neurotrophic factor signaling.BMC biology · 2021Article
- Spine dynamics in the brain, mental disorders and artificial neural networks.Nature reviews. Neuroscience · 2021Review
- Review
- The soluble neurexin-1β ectodomain causes calcium influx and augments dendritic outgrowth and synaptic transmission.Scientific reports · 2020Article
- Activity Dependent and Independent Determinants of Synaptic Size Diversity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Neuroligins Differentially Mediate Subtype-Specific Synapse Formation in Pyramidal Neurons and Interneurons.Neuroscience bulletin · 2019Article
- Article
- Relationship Between Synaptic AMPAR and Spine Dynamics: Impairments in the FXS Mouse.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Cooperative stochastic binding and unbinding explain synaptic size dynamics and statistics.PLoS computational biology · 2017Article
- Relative Contributions of Specific Activity Histories and Spontaneous Processes to Size Remodeling of Glutamatergic Synapses.PLoS biology · 2016Article
- Remodeling and Tenacity of Inhibitory Synapses: Relationships with Network Activity and Neighboring Excitatory Synapses.PLoS computational biology · 2015Article
- Synaptic size dynamics as an effectively stochastic process.PLoS computational biology · 2014Article
- Dynamic mechanisms of neuroligin-dependent presynaptic terminal assembly in living cortical neurons.Neural development · 2014Article
- The role of ionotropic glutamate receptors in childhood neurodevelopmental disorders: autism spectrum disorders and fragile x syndrome.Current neuropharmacology · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroligins (Nlgns) are postsynaptic, integral membrane cell adhesion molecules that play important roles in the formation, validation, and maturation of synapses in the mammalian central nervous system. Given their prominent roles in the life cycle of synapses, it might be expected that the loss of neuroligin family members would affect the stability of synaptic organization, and ultimately, affect the tenacity and persistence of individual synaptic junctions. Here we examined whether and to what extent the loss of Nlgn-1 affects the dynamics of several key synaptic molecules and the constancy of their contents at individual synapses over time. Fluorescently tagged versions of the postsynaptic scaffold molecule PSD-95, the AMPA-type glutamate receptor subunit GluA2 and the presynaptic vesicle molecule SV2A were expressed in primary cortical cultures from Nlgn-1 KO mice and wild-type (WT) littermates, and live imaging was used to follow the constancy of their contents at individual synapses over periods of 8-12 hours. We found that the loss of Nlgn-1 was associated with larger fluctuations in the synaptic contents of these molecules and a poorer preservation of their contents at individual synapses. Furthermore, rates of synaptic turnover were somewhat greater in neurons from Nlgn-1 knockout mice. Finally, the increased GluA2 redistribution rates observed in neurons from Nlgn-1 knockout mice were negated by suppressing spontaneous network activity. These findings suggest that the loss of Nlgn-1 is associated with some use-dependent destabilization of excitatory synapse organization, and indicate that in the absence of Nlgn-1, the tenacity of excitatory synapses might be somewhat impaired.
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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.