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Nat Commun. 2019 Mar 6;10(1):1085. doi: 10.1038/s41467-019-08977-6.

Rapid active zone remodeling consolidates presynaptic potentiation.

Author information

1
Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), 13125, Berlin, Germany.
2
NeuroCure Cluster of Excellence, Charité Universitätsmedizin, 10117, Berlin, Germany.
3
Institute for Biology/Genetics, Freie Universität Berlin, 14195, Berlin, Germany.
4
Department of Neurobiology, University of Southern California, Los Angeles, CA, 90089, USA.
5
Institut für Neurophysiologie, Charité Universitätsmedizin, 10117, Berlin, Germany.
6
Department of Theory and Bio-systems, Max Planck Institute of Colloids and Interfaces, Science Park Golm, 14424, Potsdam, Germany.
7
Department of Nanobiophotonics, Max Planck Institute for Biophysical Chemistry, 37077, Göttingen, Germany.
8
Buck Institute for Research on Aging, Novato, CA, USA.
9
NeuroCure Cluster of Excellence, Charité Universitätsmedizin, 10117, Berlin, Germany. stephan.sigrist@fu-berlin.de.
10
Institute for Biology/Genetics, Freie Universität Berlin, 14195, Berlin, Germany. stephan.sigrist@fu-berlin.de.
11
Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), 13125, Berlin, Germany. awalter@fmp-berlin.de.

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.

PMID:
30842428
PMCID:
PMC6403334
DOI:
10.1038/s41467-019-08977-6
[Indexed for MEDLINE]
Free PMC Article

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