ArticleScientific reports2019
Synaptotagmin-1 enables frequency coding by suppressing asynchronous release in a temperature dependent manner.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Impact of distinct neurotransmitter release modes on neuronal signaling.Molecular psychiatry · 2026Review
- Encoding opposing valences through frequency-dependent transmitter switching in single peptidergic neurons.bioRxiv : the preprint server for biology · 2024Article
- A de novo missense mutation in synaptotagmin-1 associated with neurodevelopmental disorder desynchronizes neurotransmitter release.Molecular psychiatry · 2024Article
- Parallel processing of quickly and slowly mobilized reserve vesicles in hippocampal synapses.eLife · 2024Article
- Asynchronous glutamate release is enhanced in low release efficacy synapses and dispersed across the active zone.Nature communications · 2022Article
- Article
- Diverse roles of Synaptotagmin-7 in regulating vesicle fusion.Current opinion in neurobiology · 2020Review
- Article
- Temperature effects on synaptic transmission and neuronal function in the visual thalamus.PloS one · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To support frequency-coded information transfer, mammalian synapses tightly synchronize neurotransmitter release to action potentials (APs). However, release desynchronizes during AP trains, especially at room temperature. Here we show that suppression of asynchronous release by Synaptotagmin-1 (Syt1), but not release triggering, is highly temperature sensitive, and enhances synchronous release during high-frequency stimulation. In Syt1-deficient synapses, asynchronous release increased with temperature, opposite to wildtype synapses. Mutations in Syt1 C2B-domain polybasic stretch (Syt1 K326Q,K327Q,K331Q) did not affect synchronization during sustained activity, while the previously observed reduced synchronous response to a single AP was confirmed. However, an inflexible linker between the C2-domains (Syt1 9Pro) reduced suppression, without affecting synchronous release upon a single AP. Syt1 9Pro expressing synapses showed impaired synchronization during AP trains, which was rescued by buffering global Ca
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