PUBLICATION

Distinct roles for two synaptotagmin isoforms in synchronous and asynchronous transmitter release at zebrafish neuromuscular junction

Authors
Wen, H., Linhoff, M.W., McGinley, M.J., Li, G.L., Corson, G.M., Mandel, G., and Brehm, P.
ID
ZDB-PUB-100726-11
Date
2010
Source
Proceedings of the National Academy of Sciences of the United States of America   107(31): 13906-13911 (Journal)
Registered Authors
Keywords
active zone, exocytosis, synapse, acetylcholine receptor
MeSH Terms
  • Animals
  • Molecular Sequence Data
  • Neuromuscular Junction/metabolism*
  • Protein Isoforms/genetics
  • Protein Isoforms/metabolism
  • Synaptic Transmission*
  • Synaptotagmins/genetics
  • Synaptotagmins/metabolism*
  • Transcription, Genetic
  • Zebrafish/metabolism*
PubMed
20643933 Full text @ Proc. Natl. Acad. Sci. USA
Abstract
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
Figures
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Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes