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Acute complexin knockout abates spontaneous and evoked transmitter release

MPS-Authors

López-Murcia,  Francisco José
Molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Reim,  Kerstin
Molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Jahn,  Olaf
Proteomics, Wiss. Servicegruppen, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Taschenberger,  Holger       
Molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Brose,  Nils
Molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Citation

López-Murcia, F. J., Reim, K., Jahn, O., Taschenberger, H., & Brose, N. (2019). Acute complexin knockout abates spontaneous and evoked transmitter release. Cell Reports, 26(10), 2521-2530.e5. doi:10.1016/j.celrep.2019.02.030.


Cite as: https://hdl.handle.net/21.11116/0000-0003-21B5-B
Abstract
SNARE-mediated synaptic vesicle (SV) fusion is controlled by multiple regulatory proteins that determine neurotransmitter release efficiency. Complexins are essential SNARE regulators whose mode of action is unclear, as available evidence indicates positive SV fusion facilitation and negative “fusion clamp”-like activities, with the latter occurring only in certain contexts. Because these contradictory findings likely originate in part from different experimental perturbation strategies, we attempted to resolve them by examining a conditional complexin-knockout mouse line as the most stringent genetic perturbation model available. We found that acute complexin loss after synaptogenesis in autaptic and mass-cultured hippocampal neurons reduces SV fusion probability and thus abates the rates of spontaneous, synchronous, asynchronous, and delayed transmitter release but does not affect SV priming or cause “unclamping” of spontaneous SV fusion. Thus, complexins act as facilitators of SV fusion but are dispensable for “fusion clamping” in mammalian forebrain neurons.