Distinct roles for two synaptotagmin isoforms in synchronous and asynchronous transmitter release at zebrafish neuromuscular junction
- Wen, H., Linhoff, M.W., McGinley, M.J., Li, G.L., Corson, G.M., Mandel, G., and Brehm, P.
- Proceedings of the National Academy of Sciences of the United States of America 107(31): 13906-13911 (Journal)
- Registered Authors
- active zone, exocytosis, synapse, acetylcholine receptor
- MeSH Terms
- Molecular Sequence Data
- Neuromuscular Junction/metabolism*
- Protein Isoforms/genetics
- Protein Isoforms/metabolism
- Synaptic Transmission*
- Transcription, Genetic
- 20643933 Full text @ Proc. Natl. Acad. Sci. USA
Wen, H., Linhoff, M.W., McGinley, M.J., Li, G.L., Corson, G.M., Mandel, G., and Brehm, P. (2010) Distinct roles for two synaptotagmin isoforms in synchronous and asynchronous transmitter release at zebrafish neuromuscular junction. Proceedings of the National Academy of Sciences of the United States of America. 107(31):13906-13911.
An obligatory role for the calcium sensor synaptotagmins in stimulus-coupled release of neurotransmitter is well established, but a role for synaptotagmin isoform involvement in asynchronous release remains conjecture. We show, at the zebrafish neuromuscular synapse, that two separate synaptotagmins underlie these processes. Specifically, knockdown of synaptotagmin 2 (syt2) reduces synchronous release, whereas knockdown of synaptotagmin 7 (syt7) reduces the asynchronous component of release. The zebrafish neuromuscular junction is unique in having a very small quantal content and a high release probability under conditions of either low-frequency stimulation or high-frequency augmentation. Through these features, we further determined that during the height of shared synchronous and asynchronous transmission these two modes compete for the same release sites.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes