ArticleProceedings of the National Academy of Sciences of the United States of America2007
Posttetanic potentiation critically depends on an enhanced Ca(2+) sensitivity of vesicle fusion mediated by presynaptic PKC.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 90 citations in OpenAlex.
- Munc13-1 couples DAG and CaScience advances · 2026Article
- Mechanistic insights into cAMP-mediated presynaptic potentiation at hippocampal mossy fiber synapses.Frontiers in cellular neuroscience · 2023Review
- Presynaptic Short-Term Plasticity Persists in the Absence of PKC Phosphorylation of Munc18-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Imaging the Nanoscale Distribution of Phosphoinositides in the Cell Plasma Membrane with Single-Molecule Localization Super-Resolution Microscopy.Methods in molecular biology (Clifton, N.J.) · 2021Article
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- The Onset and Progression of Hippocampal Synaptic Plasticity Deficits in the Q175FDN Mouse Model of Huntington Disease.Frontiers in cellular neuroscience · 2019Article
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- Persistent but Labile Synaptic Plasticity at Excitatory Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Single Bursts of Individual Granule Cells Functionally Rearrange Feedforward Inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Molecular Mechanisms of Short-Term Plasticity: Role of Synapsin Phosphorylation in Augmentation and Potentiation of Spontaneous Glutamate Release.Frontiers in synaptic neuroscience · 2018Article
- BDNF-TrkB Signaling Coupled to nPKCε and cPKCβI Modulate the Phosphorylation of the Exocytotic Protein Munc18-1 During Synaptic Activity at the Neuromuscular Junction.Frontiers in molecular neuroscience · 2018Article
- A single episode of high intensity sound inhibits long-term potentiation in the hippocampus of rats.Scientific reports · 2017Article
- SNAP-25 phosphorylation at Ser187 regulates synaptic facilitation and short-term plasticity in an age-dependent manner.Scientific reports · 2017Article
- Article
- Dynamin-1 deletion enhances post-tetanic potentiation and quantal size after tetanic stimulation at the calyx of Held.The Journal of physiology · 2017Article
- The calyx of Held in the auditory system: Structure, function, and development.Hearing research · 2016Review
- Calcium-Dependent Protein Kinase C Is Not Required for Post-Tetanic Potentiation at the Hippocampal CA3 to CA1 Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Phosphorylation of synaptotagmin-1 controls a post-priming step in PKC-dependent presynaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Extremely Low Frequency Electromagnetic Fields Facilitate Vesicle Endocytosis by Increasing Presynaptic Calcium Channel Expression at a Central Synapse.Scientific reports · 2016Article
- Molecular Machines Regulating the Release Probability of Synaptic Vesicles at the Active Zone.Frontiers in synaptic neuroscience · 2016Review
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activity-dependent enhancement of transmitter release is a common form of presynaptic plasticity, but the underlying signaling mechanisms have remained largely unknown, perhaps because of the inaccessibility of most CNS nerve terminals. Here we investigated the signaling steps that underlie posttetanic potentiation (PTP), a form of presynaptic plasticity found at many CNS synapses. Direct whole-cell recordings from the large calyx of Held nerve terminals with the perforated patch-clamp technique showed that PTP was not mediated by changes in the presynaptic action potential waveform. Ca(2+) imaging revealed a slight increase of the presynaptic Ca(2+) transient during PTP ( approximately 15%), which, however, was too small to explain a large part of PTP. The presynaptic PKC pathway was critically involved in PTP because (i) PTP was occluded by activation of PKC with phorbol esters, and (ii) PTP was largely (by approximately two-thirds) blocked by the PKC inhibitors, Ro31-8220 or bisindolylmaleimide. Activation of PKC during PTP most likely acts directly on the presynaptic release machinery, because in presynaptic Ca(2+) uncaging experiments, activation of PKC by phorbol ester greatly increased the Ca(2+) sensitivity of vesicle fusion in a Ro31-8220-sensitive manner ( approximately 300% with small Ca(2+) uncaging stimuli), but only slightly increased presynaptic voltage-gated Ca(2+) currents ( approximately 15%). We conclude that a PKC-dependent increase in the Ca(2+) sensitivity of vesicle fusion is a key step in the enhancement of transmitter release during PTP.
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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.