2026-04-20T03:03:20Zhttps://recercat.cat/oai/requestoai:recercat.cat:2445/2287172026-04-09T05:41:44Zcom_2072_1057col_2072_478916col_2072_478929
RECERCAT
author
López Murcia, Francisco José
author
Krueger-Burg, Dilja
author
Wenger, Sally
author
López Hernández, Tania
author
Lipstein, Noa
author
Taschenberger, Holger
author
Brose, Nils
2026-04-09T05:41:43Z
2026-04-09T05:41:43Z
2026-04-08T10:21:08Z2026-04-08T10:21:08Z2026-02-192026-04-08T10:21:08Z
https://hdl.handle.net/2445/228717
Hippocampal mossy fiber (hMF) to CA3 pyramidal cell synapses are thought to support the formation of working memory through presynaptic short-term facilitation (STF) and post-tetanic potentiation (PTP). However, the molecular mechanisms underlying these transient forms of synaptic enhancement are unclear. We show here that Munc13-1-mediated priming of synaptic vesicles (SVs) at active zones controls hMF STF and PTP in response to Ca2+-phospholipid and Ca2+-calmodulin (CaM) signaling. Knock-in mice expressing Munc13-1 variants insensitive to either signaling pathway exhibit pronounced deficits in STF and PTP, and the PTP-induction threshold is markedly increased upon block of Ca2+-phospholipid-Munc13-1 signaling. Since these synaptic defects are accompanied by working memory deficits, especially in mice expressing the Ca2+-phospholipid-insensitive Munc13-1 variant, we conclude that the Ca2+-dependent regulation of Munc13-1-mediated SV priming co-determines hMF short-term plasticity and working memory formation.
cc-by (c) López-Murcia, F.J. et al., 2026 http://creativecommons.org/licenses/by/4.0/ info:eu-repo/semantics/openAccess
Antagonistes del calci
Sinapsi
Regulació cel·lular
Calcium antagonists
Synapses
Cellular control mechanisms
Ca2+-phospholipid–dependent regulation of Munc13-1 is essential for post-tetanic potentiation at mossy fiber synapses and supports working memory.
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion