ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Opposing action of nuclear factor κB and Polo-like kinases determines a homeostatic end point for excitatory synaptic adaptation.
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 17 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
17 citing papers in PubMed, 27 citations in OpenAlex.
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- Cataloguing and Selection of mRNAs Localized to Dendrites in Neurons and Regulated by RNA-Binding Proteins in RNA Granules.Biomolecules · 2020Review
- iTRAQ-Based Protein Profiling in CUMS Rats Provides Insights into Hippocampal Ribosome Lesion and Ras Protein Changes Underlying Synaptic Plasticity in Depression.Neural plasticity · 2019Article
- Cellular Specificity of NF-κB Function in the Nervous System.Frontiers in immunology · 2019Review
- Dysregulation and restoration of homeostatic network plasticity in fragile X syndrome mice.Neuropharmacology · 2018Article
- Targeting of NF-κB to Dendritic Spines Is Required for Synaptic Signaling and Spine Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Imbalance between firing homeostasis and synaptic plasticity drives early-phase Alzheimer's disease.Nature neuroscience · 2018Review
- Exosomes and Homeostatic Synaptic Plasticity Are Linked to Each other and to Huntington's, Parkinson's, and Other Neurodegenerative Diseases by Database-Enabled Analyses of Comprehensively Curated Datasets.Frontiers in neuroscience · 2017Article
- NFκB-inducing kinase inhibits NFκB activity specifically in neurons of the CNS.Journal of neurochemistry · 2016Article
- Feedback modulation of neural network synchrony and seizure susceptibility by Mdm2-p53-Nedd4-2 signaling.Molecular brain · 2016Article
- Neuronal Gene Targets of NF-κB and Their Dysregulation in Alzheimer's Disease.Frontiers in molecular neuroscience · 2016Review
- The Shank3 Interaction Partner ProSAPiP1 Regulates Postsynaptic SPAR Levels and the Maturation of Dendritic Spines in Hippocampal Neurons.Frontiers in synaptic neuroscience · 2016Article
- The role of the ubiquitin-editing enzyme A20 in diseases of the central nervous system and other pathological processes.Frontiers in molecular neuroscience · 2015Review
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Homeostatic responses critically adjust synaptic strengths to maintain stability in neuronal networks. Compensatory adaptations to prolonged excitation include induction of Polo-like kinases (Plks) and degradation of spine-associated Rap GTPase-activating protein (SPAR) to reduce synaptic excitation, but mechanisms that limit overshooting and allow refinement of homeostatic adjustments remain poorly understood. We report that Plks produce canonical pathway-mediated activation of the nuclear factor κB (NF-κB) transcription factor in a process that requires the kinase activity of Plks. Chronic elevated activity, which induces Plk expression, also produces Plk-dependent activation of NF-κB. Deficiency of NF-κB, in the context of exogenous Plk2 expression or chronic elevated neuronal excitation, produces exaggerated homeostatic reductions in the size and density of dendritic spines, synaptic AMPA glutamate receptor levels, and excitatory synaptic currents. During the homeostatic response to chronic elevated activity, NF-κB activation by Plks subsequently opposes Plk-mediated SPAR degradation by transcriptionally upregulating SPAR in mouse hippocampal neurons in vitro and in vivo. Exogenous SPAR expression can rescue the overshooting of homeostatic reductions at excitatory synapses in NF-κB-deficient neurons responding to elevated activity. Our data establish an integral feedback loop involving NF-κB, Plks, and SPAR that regulates the end point of homeostatic synaptic adaptation to elevated activity and are the first to implicate a transcription factor in the regulation of homeostatic synaptic responses.
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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.