ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Synaptic vesicles in mature calyx of Held synapses sense higher nanodomain calcium concentrations during action potential-evoked glutamate release.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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74 citing papers in PubMed.
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- Synaptic Vesicle Recycling at the Developing Presynapse.Journal of neurochemistry · 2025Review
- How SNARE proteins generate force to fuse membranes.Biophysical journal · 2025Article
- Cellular and synaptic specializations for sub-millisecond precision in the mammalian auditory brainstem.Frontiers in cellular neuroscience · 2025Review
- Human iPSC-Derived Neurons with Reliable Synapses and Large Presynaptic Action Potentials.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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
- Synaptotagmin 7 docks synaptic vesicles to support facilitation and Doc2α-triggered asynchronous release.eLife · 2024Article
- Caged ZnACS chemical neuroscience · 2024Article
- CaEMBO reports · 2022Article
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- Presynaptic Rac1 controls synaptic strength through the regulation of synaptic vesicle priming.eLife · 2022Article
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- Regulation of presynaptic CaeLife · 2022Article
- Mechanisms controlling the trafficking, localization, and abundance of presynaptic CaFrontiers in molecular neuroscience · 2022Review
- Influence of T-Bar on Calcium Concentration Impacting Release Probability.Frontiers in computational neuroscience · 2022Article
- Article
14 more citing papers are in PubMed but not listed here.
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3 authors.
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Abstract
During development of the calyx of Held synapse, presynaptic action potentials (APs) become substantially faster and briefer. Nevertheless, this synapse is able to upregulate quantal output triggered by arriving APs. Briefer APs lead to less effective gating of voltage-gated Ca(2+) channels (VGCCs). Therefore, mechanisms downstream of Ca(2+) entry must effectively compensate for the attenuated Ca(2+) influx associated with shorter APs in more mature calyces. This compensation could be achieved by tighter spatial coupling between VGCCs and synaptic vesicles, so that the latter are exposed to higher intracellular Ca(2+) concentration ([Ca(2+)](i)). Alternatively or additionally, the Ca(2+) sensitivity of the release apparatus may increase during synapse development. To differentiate between these possibilities, we combined paired patch-clamp recordings with Ca(2+) imaging and flash photolysis of caged Ca(2+) and estimated the [Ca(2+)](i) requirements for vesicle release in the developing mouse calyx of Held synapse. Surprisingly, the dose-response relationship between [Ca(2+)](i) and release rate was shifted slightly to the right in more mature calyces, rendering their vesicles slightly less sensitive to incoming Ca(2+). Taking into account the time course and peak rates of AP-evoked release transients for the corresponding developmental stages, we estimate the local [Ca(2+)](i)"seen" by the Ca(2+) sensors on synaptic vesicles to increase from 35 to 56 mum [from postnatal day 9 (P9)-P11 to P16-P19]. Our results reinforce the idea that developmental tightening of the spatial coupling between VGCCs and synaptic vesicles plays a predominant role in enhancing quantal output at this synapse and possibly other central synapses.
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