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725949.pdf (3.67 MB)

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Data de publicació

2019-03

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cc-by (c) López-Murcia, Francisco José et al., 2019
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/196447

Acute complexin knockout abates spontaneous and evoked transmitter release

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Recurs relacionat

https://doi.org/10.1016/j.celrep.2019.02.030

Resum

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.

Matèries

Neurotransmissió, Ratolins (Animals de laboratori), Proteïnes SNARE

Matèries (anglès)

Neural transmission, Mice (Laboratory animals), SNARE Proteins

Citació

Col·leccions

Articles publicats en revistes (Patologia i Terapèutica Experimental)

Citació

LÓPEZ-MURCIA, Francisco José, et al. Acute complexin knockout abates spontaneous and evoked transmitter release. Cell Reports. 2019. Vol. 26, num. 10. ISSN 2211-1247. [consulted: 3 of August of 2026]. Available at: https://hdl.handle.net/2445/196447

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