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A complexin fusion clamp regulates spontaneous neurotransmitter release and synaptic growth

Abstract

Neuronal signaling occurs through both action potential–triggered synaptic vesicle fusion and spontaneous release, although the fusion clamp machinery that prevents premature exocytosis of synaptic vesicles in the absence of calcium is unknown. Here we demonstrate that spontaneous release at synapses is regulated by complexin, a SNARE complex–binding protein. Analysis of Drosophila melanogaster complexin null mutants showed a marked increase in spontaneous fusion and a profound overgrowth of synapses, suggesting that complexin functions as the fusion clamp in vivo and may modulate structural remodeling of neuronal connections by controlling the rate of spontaneous release.

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Figure 1: Generation of complexin mutants in Drosophila.
Figure 2: complexin mutants show a marked increase in mini frequency at third-instar larval NMJs.
Figure 3: complexin mutant NMJs show synaptic overgrowth.

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Acknowledgements

We thank A. Rodal and R. Rodriguez for discussions. This work was supported by grants from the US National Institutes of Health and the Packard Foundation.

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S.H. and J.T.L. performed the experiments and wrote the manuscript.

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Correspondence to J Troy Littleton.

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Supplementary Figures 1–3, Supplementary Methods (PDF 3725 kb)

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Huntwork, S., Littleton, J. A complexin fusion clamp regulates spontaneous neurotransmitter release and synaptic growth. Nat Neurosci 10, 1235–1237 (2007). https://doi.org/10.1038/nn1980

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