Complexin has opposite effects on two modes of synaptic vesicle fusion

Martin, Jesse A., Hu, Zhitao, Fenz, Katherine M., Fernandez, Joel and Dittman, Jeremy S. (2011) Complexin has opposite effects on two modes of synaptic vesicle fusion. Current Biology, 21 2: 97-105. doi:10.1016/j.cub.2010.12.014

Author Martin, Jesse A.
Hu, Zhitao
Fenz, Katherine M.
Fernandez, Joel
Dittman, Jeremy S.
Title Complexin has opposite effects on two modes of synaptic vesicle fusion
Journal name Current Biology   Check publisher's open access policy
ISSN 0960-9822
Publication date 2011-01-25
Sub-type Article (original research)
DOI 10.1016/j.cub.2010.12.014
Open Access Status Not yet assessed
Volume 21
Issue 2
Start page 97
End page 105
Total pages 9
Place of publication Cambridge, MA, United States
Publisher Cell Press
Language eng
Formatted abstract

Synaptic transmission can occur in a binary or graded fashion, depending on whether transmitter release is triggered by action potentials or by gradual changes in membrane potential. Molecular differences of these two types of fusion events and their differential regulation in a physiological context have yet to be addressed. Complexin is a conserved SNARE-binding protein that has been proposed to regulate both spontaneous and stimulus-evoked synaptic vesicle (SV) fusion.


Here we examine complexin function at a graded synapse in C. elegans. Null complexin (cpx-1) mutants are viable, although nervous system function is significantly impaired. Loss of CPX-1 results in a 3-fold increase in the rate of tonic synaptic transmission at the neuromuscular junction, whereas stimulus-evoked SV fusion is decreased 10-fold. A truncated CPX-1 missing its C-terminal domain can rescue stimulus-evoked synaptic vesicle exocytosis but fails to suppress tonic activity, demonstrating that these two modes of exocytosis can be distinguished at the molecular level. A CPX-1 variant with impaired SNARE binding also rescues evoked, but not tonic, neurotransmitter release. Finally, tonic, but not evoked, release can be rescued in a syntaxin point mutant by removing CPX-1. Rescue of either form of exocytosis partially restores locomotory behavior, indicating that both types of synaptic transmission are relevant.


These observations suggest a dual role for CPX-1: suppressing SV exocytosis, driven by low levels of endogenous neural activity, while promoting synchronous fusion of SVs driven by a depolarizing stimulus. Thus, patterns of synaptic activity regulate complexin's inhibitory and permissive roles at a graded synapse.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Queensland Brain Institute Publications
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Citation counts: TR Web of Science Citation Count  Cited 66 times in Thomson Reuters Web of Science Article | Citations
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