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RIM-Binding Protein Links Synaptic Homeostasis to the Stabilization and Replenishment of High Release Probability Vesicles


Müller, Martin; Genç, Özgür; Davis, Graeme W (2015). RIM-Binding Protein Links Synaptic Homeostasis to the Stabilization and Replenishment of High Release Probability Vesicles. Neuron, 85(5):1056-1069.

Abstract

Here we define activities of RIM-binding protein (RBP) that are essential for baseline neurotransmission and presynaptic homeostatic plasticity. At baseline, rbp mutants have a ∼10-fold decrease in the apparent Ca2+ sensitivity of release that we attribute to (1) impaired presynaptic Ca2+ influx, (2) looser coupling of vesicles to Ca2+ influx, and (3) limited access to the readily releasable vesicle pool (RRP). During homeostatic plasticity, RBP is necessary for the potentiation of Ca2+ influx and the expansion of the RRP. Remarkably, rbp mutants also reveal a rate-limiting stage required for the replenishment of high release probability (p) vesicles following vesicle depletion. This rate slows ∼4-fold at baseline and nearly 7-fold during homeostatic signaling in rbp. These effects are independent of altered Ca2+ influx and RRP size. We propose that RBP stabilizes synaptic efficacy and homeostatic plasticity through coordinated control of presynaptic Ca2+ influx and the dynamics of a high-p vesicle pool.

Abstract

Here we define activities of RIM-binding protein (RBP) that are essential for baseline neurotransmission and presynaptic homeostatic plasticity. At baseline, rbp mutants have a ∼10-fold decrease in the apparent Ca2+ sensitivity of release that we attribute to (1) impaired presynaptic Ca2+ influx, (2) looser coupling of vesicles to Ca2+ influx, and (3) limited access to the readily releasable vesicle pool (RRP). During homeostatic plasticity, RBP is necessary for the potentiation of Ca2+ influx and the expansion of the RRP. Remarkably, rbp mutants also reveal a rate-limiting stage required for the replenishment of high release probability (p) vesicles following vesicle depletion. This rate slows ∼4-fold at baseline and nearly 7-fold during homeostatic signaling in rbp. These effects are independent of altered Ca2+ influx and RRP size. We propose that RBP stabilizes synaptic efficacy and homeostatic plasticity through coordinated control of presynaptic Ca2+ influx and the dynamics of a high-p vesicle pool.

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12 citations in Web of Science®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:07 Faculty of Science > Institute of Molecular Life Sciences
Dewey Decimal Classification:570 Life sciences; biology
Language:English
Date:4 March 2015
Deposited On:25 Feb 2016 08:10
Last Modified:05 Apr 2016 20:10
Publisher:Cell Press (Elsevier)
ISSN:0896-6273
Funders:Swiss National Science Foundation Fellowship PBSKP3-123456/1 (M.M.), National Institutes of Health Grants NS39313 and NS059867 (G.W.D.)
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/j.neuron.2015.01.024

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