ArticleProceedings of the National Academy of Sciences of the United States of America2023
Fully-primed slowly-recovering vesicles mediate presynaptic LTP at neocortical neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 17 citations in OpenAlex.
- A computational theory of short-term synaptic plasticity: synapses learn to tell time.Research square · 2026Article
- Caloric restriction decelerates premature aging and cognitive decline in mice with deficient DNA repair.Communications biology · 2026Article
- Selective, genetically induced increase in synaptic vesicle priming.Science advances · 2026Article
- Munc13-1 couples DAG and CaScience advances · 2026Article
- The perforant pathway and CA3-Schaffer collateral afferents coordinate to regulate spatial learning.Communications biology · 2026Article
- Interactions between long- and short-term synaptic plasticity transform temporal neural representations into spatial.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Number and relative abundance of synaptic vesicles in functionally distinct priming states determine synaptic strength and short-term plasticity.The Journal of physiology · 2025Article
- Inferring synaptic transmission from the stochastic dynamics of the quantal content: An analytical approach.PLoS computational biology · 2025Article
- Estimates of quantal synaptic parameters in light of more complex vesicle pool models.Frontiers in cellular neuroscience · 2025Article
- Different states of synaptic vesicle priming explain target cell type-dependent differences in neurotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Complexin has a dual synaptic function as checkpoint protein in vesicle priming and as a promoter of vesicle fusion.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Tomosyns attenuate SNARE assembly and synaptic depression by binding to VAMP2-containing template complexes.Nature communications · 2024Article
- Interpretation of presynaptic phenotypes of synaptic plasticity in terms of a two-step priming process.The Journal of general physiology · 2024Article
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11 authors at 2 institutions in 1 country.
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Abstract
Pre- and postsynaptic forms of long-term potentiation (LTP) are candidate synaptic mechanisms underlying learning and memory. At layer 5 pyramidal neurons, LTP increases the initial synaptic strength but also short-term depression during high-frequency transmission. This classical form of presynaptic LTP has been referred to as redistribution of synaptic efficacy. However, the underlying mechanisms remain unclear. We therefore performed whole-cell recordings from layer 5 pyramidal neurons in acute cortical slices of rats and analyzed presynaptic function before and after LTP induction by paired pre- and postsynaptic neuronal activity. LTP was successfully induced in about half of the synaptic connections tested and resulted in increased synaptic short-term depression during high-frequency transmission and a decelerated recovery from short-term depression due to an increased fraction of a slow recovery component. Analysis with a recently established sequential two-step vesicle priming model indicates an increase in the abundance of fully-primed and slowly-recovering vesicles. A systematic analysis of short-term plasticity and synapse-to-synapse variability of synaptic strength at various types of synapses revealed that stronger synapses generally recover more slowly from synaptic short-term depression. Finally, pharmacological stimulation of the cyclic adenosine monophosphate and diacylglycerol signaling pathways, which are both known to promote synaptic vesicle priming, mimicked LTP and slowed the recovery from short-term depression. Our data thus demonstrate that LTP at layer 5 pyramidal neurons increases synaptic strength primarily by enlarging a subpool of fully-primed slowly-recovering vesicles.
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