ArticleCell reports2018
Genetic Dissection of Presynaptic and Postsynaptic BDNF-TrkB Signaling in Synaptic Efficacy of CA3-CA1 Synapses.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 108 citations in OpenAlex.
- Article
- Molecular architects of memory: BDNF/TrkB signaling and trafficking in neuronal plasticity and memory.Molecular psychiatry · 2026Review
- The synaptic triad in depression: how stress-related pathways converge on BDNF, NMDA receptor, and MMP-9.Pharmacological reports : PR · 2026Review
- Functional Nano-segregation of Distinct Forms of Neurotransmission.Advances in neurobiology · 2026Review
- Orexins and neuregulins as exemplars of peptide physiology in the brain: experimental challenges and implications for neuropathology.Frontiers in cellular neuroscience · 2026Article
- BDNF-driven synaptic plasticity requires autocrine matrix metalloproteinase-9 activity.Science advances · 2025Article
- Synaptic signatures of perinatal cannabinoids: A systematic review of rodent hippocampal synaptic plasticity, learning, and memory.Drug and alcohol dependence reports · 2025Review
- Synaptic basis of rapid antidepressant action.European archives of psychiatry and clinical neuroscience · 2025Review
- Enhancing Functional Recovery After Spinal Cord Injury Through Neuroplasticity: A Comprehensive Review.International journal of molecular sciences · 2025Review
- MeCP2 prevents against sustained ketamine-induced synaptic depression at inhibitory synapses.iScience · 2025Article
- Enhanced ERK activity extends ketamine's antidepressant effects by augmenting synaptic plasticity.Science (New York, N.Y.) · 2025Article
- Role of brain-derived neurotrophic factor in dysfunction of short-term to long-term memory transformation after surgery and anaesthesia in older mice.British journal of anaesthesia · 2025Article
- B cells upregulate NMDARs, respond to extracellular glutamate, and express mature BDNF to protect the brain from ischemic injury.Neurobiology of disease · 2025Article
- BDNF Signaling and Pain Modulation.Cells · 2025Review
- Altered synaptic homeostasis: a key factor in the pathophysiology of depression.Cell & bioscience · 2025Review
- The CHD Protein, Kismet, Restricts Synaptic BMP Signaling at Glutamatergic Synapses.Neuroscience insights · 2025Article
- Lactate infusion increases circulating pro-brain-derived neurotrophic factor levels in humans.Frontiers in cellular neuroscience · 2025Article
- Multi-target approach of Egyptian leek extract in ameliorating depressive-like behavior in rats exposed to chronic unpredictable mild stress.Frontiers in pharmacology · 2025Article
- Axonopathy Underlying Amyotrophic Lateral Sclerosis: Unraveling Complex Pathways and Therapeutic Insights.Neuroscience bulletin · 2024Review
- BDNF-dependent nano-organization of Neogenin and the WAVE regulatory complex promotes actin remodeling in dendritic spines.iScience · 2024Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, tropomyosin receptor kinase B (TrkB), regulate long-term potentiation (LTP) in the hippocampus, although the sites of BDNF-TrkB receptors in this process are controversial. We used a viral-mediated approach to delete BDNF or TrkB specifically in CA1 and CA3 regions of the Schaffer collateral pathway. Deletion of BDNF in CA3 or CA1 revealed that presynaptic BDNF is involved in LTP induction, while postsynaptic BDNF contributes to LTP maintenance. Similarly, loss of presynaptic or postsynaptic TrkB receptors leads to distinct LTP deficits, with presynaptic TrkB required to maintain LTP, while postsynaptic TrkB is essential for LTP formation. In addition, loss of TrkB in CA3 significantly diminishes release probability, uncovering a role for presynaptic TrkB receptors in basal neurotransmission. Taken together, this direct comparison of presynaptic and postsynaptic BDNF-TrkB reveals insight into BDNF release and TrkB activation sites in hippocampal LTP.
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What OpenQuestion holds
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.