ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2003
Fusion pore modulation as a presynaptic mechanism contributing to expression of long-term potentiation.
Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Fusion Pores as Regulators of Quantal Size and Cellular Physiology.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Synergistic regulation of fusion pore opening and dilation by SNARE and synaptotagmin-1.Journal of molecular cell biology · 2024Article
- Differential SNARE chaperoning by Munc13-1 and Munc18-1 dictates fusion pore fate at the release site.Nature communications · 2024Article
- Synaptic Integration of Subquantal Neurotransmission by Colocalized G Protein-Coupled Receptors in Presynaptic Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Shortened tethering filaments stabilize presynaptic vesicles in support of elevated release probability during LTP in rat hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Parsing Out the Variability of Transmission at Central Synapses Using Optical Quantal Analysis.Frontiers in synaptic neuroscience · 2019Article
- Optical Quantal Analysis.Frontiers in synaptic neuroscience · 2019Article
- Article
- Pharmacological rescue of cortical synaptic and network potentiation in a mouse model for fragile X syndrome.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- Exocytosis and endocytosis: modes, functions, and coupling mechanisms.Annual review of physiology · 2014Review
- Presynaptic ultrastructural plasticity along CA3→CA1 axons during long-term potentiation in mature hippocampus.The Journal of comparative neurology · 2013Article
- Tonic NMDA receptor-mediated current in prefrontal cortical pyramidal cells and fast-spiking interneurons.Journal of neurophysiology · 2012Article
- Influence of synaptic vesicle position on release probability and exocytotic fusion mode.Science (New York, N.Y.) · 2012Article
- Use-dependent AMPA receptor block reveals segregation of spontaneous and evoked glutamatergic neurotransmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- SNARE force synchronizes synaptic vesicle fusion and controls the kinetics of quantal synaptic transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Vesicular release of glutamate utilizes the proton gradient between the vesicle and synaptic cleft.Frontiers in synaptic neuroscience · 2010Article
- Vesicular release mode shapes the postsynaptic response at hippocampal synapses.The Journal of physiology · 2009Article
- Presynaptic G-protein-coupled receptors dynamically modify vesicle fusion, synaptic cleft glutamate concentrations, and motor behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Article
- The dynamic control of kiss-and-run and vesicular reuse probed with single nanoparticles.Science (New York, N.Y.) · 2009Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Working on the idea that postsynaptic and presynaptic mechanisms of long-term potentiation (LTP) expression are not inherently mutually exclusive, we have looked for the existence and functionality of presynaptic mechanisms for augmenting transmitter release in hippocampal slices. Specifically, we asked if changes in glutamate release might contribute to the conversion of 'silent synapses' that show N-methyl-D-aspartate (NMDA) responses but no detectable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) responses, to ones that exhibit both. Here, we review experiments where NMDA receptor responses provided a bioassay of cleft glutamate concentration, using opposition between peak [glu](cleft )and a rapidly reversible antagonist, L-AP5. We discuss findings of a dramatic increase in peak [glu](cleft) upon expression of pairing-induced LTP (Choi). We present simulations with a quantitative model of glutamatergic synaptic transmission that includes modulation of the presynaptic fusion pore, realistic cleft geometry and a distributed array of postsynaptic receptors and glutamate transporters. The modelling supports the idea that changes in the dynamics of glutamate release can contribute to synaptic unsilencing. We review direct evidence from Renger et al., in accord with the modelling, that trading off the strength and duration of the glutamate transient can markedly alter AMPA receptor responses with little effect on NMDA receptor responses. An array of additional findings relevant to fusion pore modulation and its proposed contribution to LTP expression are considered.
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