Rapid active zone remodeling consolidates presynaptic potentiation

Mathias A. Böhme, Anthony W. McCarthy, Andreas T. Grasskamp, Christine B. Beuschel, Pragya Goel, Meida Jusyte, Desiree Laber, Sheng Huang, Ulises Rey, Astrid G. Petzoldt, Martin Lehmann, Fabian Göttfert, Pejmun Haghighi, Stefan W. Hell, David Owald, Dion Dickman, Stephan J. Sigrist () and Alexander M. Walter ()
Additional contact information
Mathias A. Böhme: Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP)
Anthony W. McCarthy: Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP)
Andreas T. Grasskamp: Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP)
Christine B. Beuschel: NeuroCure Cluster of Excellence, Charité Universitätsmedizin
Pragya Goel: University of Southern California
Meida Jusyte: Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP)
Desiree Laber: Charité Universitätsmedizin
Sheng Huang: Freie Universität Berlin
Ulises Rey: Freie Universität Berlin
Astrid G. Petzoldt: Freie Universität Berlin
Martin Lehmann: Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP)
Fabian Göttfert: Max Planck Institute for Biophysical Chemistry
Pejmun Haghighi: Buck Institute for Research on Aging
Stefan W. Hell: Max Planck Institute for Biophysical Chemistry
David Owald: Charité Universitätsmedizin
Dion Dickman: University of Southern California
Stephan J. Sigrist: NeuroCure Cluster of Excellence, Charité Universitätsmedizin
Alexander M. Walter: Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP)

Nature Communications, 2019, vol. 10, issue 1, 1-16

Abstract: Abstract Neuronal communication across synapses relies on neurotransmitter release from presynaptic active zones (AZs) followed by postsynaptic transmitter detection. Synaptic plasticity homeostatically maintains functionality during perturbations and enables memory formation. Postsynaptic plasticity targets neurotransmitter receptors, but presynaptic mechanisms regulating the neurotransmitter release apparatus remain largely enigmatic. By studying Drosophila neuromuscular junctions (NMJs) we show that AZs consist of nano-modular release sites and identify a molecular sequence that adds modules within minutes of inducing homeostatic plasticity. This requires cognate transport machinery and specific AZ-scaffolding proteins. Structural remodeling is not required for immediate potentiation of neurotransmitter release, but necessary to sustain potentiation over longer timescales. Finally, mutations in Unc13 disrupting homeostatic plasticity at the NMJ also impair short-term memory when central neurons are targeted, suggesting that both plasticity mechanisms utilize Unc13. Together, while immediate synaptic potentiation capitalizes on available material, it triggers the coincident incorporation of modular release sites to consolidate synaptic potentiation.

Date: 2019
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DOI: 10.1038/s41467-019-08977-6

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