PUBLICATION
Rapid and reversible optogenetic silencing of synaptic transmission by clustering of synaptic vesicles
- Authors
- Vettkötter, D., Schneider, M., Goulden, B.D., Dill, H., Liewald, J., Zeiler, S., Guldan, J., Ateş, Y.A., Watanabe, S., Gottschalk, A.
- ID
- ZDB-PUB-221220-15
- Date
- 2022
- Source
- Nature communications 13: 78277827 (Journal)
- Registered Authors
- Schneider, Martin
- Keywords
- none
- MeSH Terms
-
- Animals
- Caenorhabditis elegans/genetics
- Cluster Analysis
- Mice
- Optogenetics*
- Synaptic Transmission/physiology
- Synaptic Vesicles*/metabolism
- Zebrafish
- PubMed
- 36535932 Full text @ Nat. Commun.
Citation
Vettkötter, D., Schneider, M., Goulden, B.D., Dill, H., Liewald, J., Zeiler, S., Guldan, J., Ateş, Y.A., Watanabe, S., Gottschalk, A. (2022) Rapid and reversible optogenetic silencing of synaptic transmission by clustering of synaptic vesicles. Nature communications. 13:78277827.
Abstract
Acutely silencing specific neurons informs about their functional roles in circuits and behavior. Existing optogenetic silencers include ion pumps, channels, metabotropic receptors, and tools that damage the neurotransmitter release machinery. While the former hyperpolarize the cell, alter ionic gradients or cellular biochemistry, the latter allow only slow recovery, requiring de novo synthesis. Thus, tools combining fast activation and reversibility are needed. Here, we use light-evoked homo-oligomerization of cryptochrome CRY2 to silence synaptic transmission, by clustering synaptic vesicles (SVs). We benchmark this tool, optoSynC, in Caenorhabditis elegans, zebrafish, and murine hippocampal neurons. optoSynC clusters SVs, observable by electron microscopy. Locomotion silencing occurs with tauon ~7.2 s and recovers with tauoff ~6.5 min after light-off. optoSynC can inhibit exocytosis for several hours, at very low light intensities, does not affect ion currents, biochemistry or synaptic proteins, and may further allow manipulating different SV pools and the transfer of SVs between them.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping