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. Petzold, Martin Lehmann, Fabian Göttfert, Pejmun Haghighi, Stefan W. Hell, David Owald, Dion Dickman, Stephan J. Sigrist, and Alexander M. Walter

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Dec 28, 2018
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Received Date: 10th December 18

Synaptic transmission is mediated by neurotransmitter release at presynaptic active zones (AZs) followed by postsynaptic neurotransmitter detection. Plastic changes in transmission maintain functionality during perturbations and enable memory formation. Postsynaptic plasticity targets neurotransmitter receptors, but presynaptic plasticity mechanisms directly regulating the neurotransmitter release apparatus remain largely enigmatic. Here we describe that AZs consist of nano-modular release site units and identify a molecular sequence adding more modules within minutes of plasticity induction. This requires cognate transport machinery and a discrete subset of AZ scaffold proteins. Structural remodeling is not required for the immediate potentiation of neurotransmitter release, but rather necessary to sustain this potentiation over longer timescales. Finally, mutations in Unc13 that disrupt homeostatic plasticity at the neuromuscular junction also impair shot-term memory when central neurons are targeted, suggesting that both forms of plasticity operate via Unc13. Together, while immediate synaptic potentiation capitalizes on available material, it triggers the coincident incorporation of modular release sites to consolidate stable synapse function.

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This is an abstract of a preprint hosted on an independent third party site. It has not been peer reviewed but is currently under consideration at Nature Communications.


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