Publisher Correction: Synaptotagmin-1 enables frequency coding by suppressing asynchronous release in a temperature dependent manner
| Autor: | L. Niels Cornelisse, Alexia Stuefer, Vincent Huson, Matthijs Verhage, Maaike A. van Boven |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
medicine.medical_specialty Hot Temperature Dependent manner Computer science lcsh:Medicine Action Potentials Synaptotagmin 1 Mice medicine Animals Point Mutation Center (algebra and category theory) lcsh:Science Cells Cultured Neurons Neurogenomics Multidisciplinary Information retrieval lcsh:R Publisher Correction Mice Inbred C57BL Asynchronous communication Synaptotagmin I Synapses Frequency coding Medical genetics lcsh:Q Calcium Female Functional genomics Gene Deletion |
| Zdroj: | Scientific Reports Scientific Reports, Vol 9, Iss 1, Pp 1-1 (2019) |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/s41598-019-54233-8 |
| Popis: | 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 |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|