ArticleNeurobiology of learning and memory2017
Long-term depression-associated signaling is required for an in vitro model of NMDA receptor-dependent synapse pruning.
Article in Neurobiology of learning and memory, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Molecular and Cellular Mechanisms of Synaptogenesis and Synaptic Refinement During Cerebellar Circuit Formation.International journal of molecular sciences · 2026Review
- The Arp2/3 complex is required for in situ haptotactic response of microglia to iC3b.EMBO reports · 2026Article
- Tau oligomers modulate synapse fate by eliciting progressive bipartite synapse dysregulation and synapse loss.Molecular neurodegeneration · 2026Article
- Microglia as hunters or gatherers of brain synapses.Nature neuroscience · 2025Review
- Neuronal activity drives PCDH9 cleavage and nuclear translocation to coordinate structural and functional remodeling.Frontiers in cellular neuroscience · 2025Article
- Oxysterols in Central and Peripheral Synaptic Communication.Advances in experimental medicine and biology · 2024Article
- Bioactive human Alzheimer brain soluble Aβ: pathophysiology and therapeutic opportunities.Molecular psychiatry · 2022Review
- Dopamine D2 receptor regulates cortical synaptic pruning in rodents.Nature communications · 2021Article
- Historical perspective and progress on protein ubiquitination at glutamatergic synapses.Neuropharmacology · 2021Review
- All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Functional repertoire of protein kinases and phosphatases in synaptic plasticity and associated neurological disorders.Neural regeneration research · 2021Review
- Maternal L-thyroxine treatment during lactation affects learning and anxiety-like behaviors but not spatial memory in adult rat progeny.Pharmacological reports : PR · 2021Article
- Article
- Caspases in the Developing Central Nervous System: Apoptosis and Beyond.Frontiers in cell and developmental biology · 2021Review
- Caspase inhibition rescues F1Fo ATP synthase dysfunction-mediated dendritic spine elimination.Scientific reports · 2020Article
- A mechanistic hypothesis for the impairment of synaptic plasticity by soluble Aβ oligomers from Alzheimer's brain.Journal of neurochemistry · 2020Review
- Neonatal ethanol exposure triggers apoptosis in the murine retrosplenial cortex: Role of inhibition of NMDA receptor-driven action potential firing.Neuropharmacology · 2020Article
- Impaired Fear Extinction Recall in Serotonin Transporter Knockout Rats Is Transiently Alleviated during Adolescence.Brain sciences · 2019Article
- Dendritic Spine Elimination: Molecular Mechanisms and Implications.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019Review
- Synaptic Elimination in Neurological Disorders.Current neuropharmacology · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Activity-dependent pruning of synaptic contacts plays a critical role in shaping neuronal circuitry in response to the environment during postnatal brain development. Although there is compelling evidence that shrinkage of dendritic spines coincides with synaptic long-term depression (LTD), and that LTD is accompanied by synapse loss, whether NMDA receptor (NMDAR)-dependent LTD is a required step in the progression toward synapse pruning is still unknown. Using repeated applications of NMDA to induce LTD in dissociated rat neuronal cultures, we found that synapse density, as measured by colocalization of fluorescent markers for pre- and postsynaptic structures, was decreased irrespective of the presynaptic marker used, post-treatment recovery time, and the dendritic location of synapses. Consistent with previous studies, we found that synapse loss could occur without apparent net spine loss or cell death. Furthermore, synapse loss was unlikely to require direct contact with microglia, as the number of these cells was minimal in our culture preparations. Supporting a model by which NMDAR-LTD is required for synapse loss, the effect of NMDA on fluorescence colocalization was prevented by phosphatase and caspase inhibitors. In addition, gene transcription and protein translation also appeared to be required for loss of putative synapses. These data support the idea that NMDAR-dependent LTD is a required step in synapse pruning and contribute to our understanding of the basic mechanisms of this developmental process.
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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.