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  Presynaptic Rac1 controls synaptic strength through the regulation of synaptic vesicle priming

Keine, C., Al-Yaari, M., Radulovic, T., Thomas, C. I., Valino Ramos, P., Guerrero-Given, D., et al. (2022). Presynaptic Rac1 controls synaptic strength through the regulation of synaptic vesicle priming. eLife. Retrieved from https://doi.org/10.7554/eLife.81505.

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Item Permalink: https://hdl.handle.net/21.11116/0000-000B-FBE1-C Version Permalink: https://hdl.handle.net/21.11116/0000-000B-FBE2-B
Genre: Journal Article
Alternative Title : eLife

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 Creators:
Keine, Christian, Author
Al-Yaari, Mohammed, Author
Radulovic, Tamara, Author
Thomas, Connon I1, Author
Valino Ramos, Paula, Author
Guerrero-Given, Debbie1, Author
Ranjan, Mrinalini, Author
Taschenberger, Holger, Author
Kamasawa, Naomi1, Author
Young Jr., Samuel M, Author
Huguenard, John R, Contributor
Affiliations:
1Max Planck Florida Institute for Neuroscience, Max Planck Society, One Max Planck Way, Jupiter FL 33458, USA, ou_1950288              

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 Abstract: Synapses contain a limited number of synaptic vesicles (SVs) that are released in response to action potentials (APs). Therefore, sustaining synaptic transmission over a wide range of AP firing rates and timescales depends on SV release and replenishment. Although actin dynamics impact synaptic transmission, how presynaptic regulators of actin signaling cascades control SV release and replenishment remains unresolved. Rac1, a Rho GTPase, regulates actin signaling cascades that control synaptogenesis, neuronal development, and postsynaptic function. However, the presynaptic role of Rac1 in regulating synaptic transmission is unclear. To unravel Rac1’s roles in controlling transmitter release, we performed selective presynaptic ablation of Rac1 at the mature mouse calyx of Held synapse. Loss of Rac1 increased synaptic strength, accelerated EPSC recovery after conditioning stimulus trains, and augmented spontaneous SV release with no change in presynaptic morphology or AZ ultrastructure. Analyses with constrained short-term plasticity models revealed faster SV priming kinetics and, depending on model assumptions, elevated SV release probability or higher abundance of tightly docked fusion-competent SVs in Rac1-deficient synapses. We conclude that presynaptic Rac1 is a key regulator of synaptic transmission and plasticity mainly by regulating the dynamics of SV priming and potentially SV release probability.

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 Dates: 2022
 Publication Status: Issued
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 Identifiers: URI: https://doi.org/10.7554/eLife.81505
URI: https://elifesciences.org/download/aHR0cHM6Ly9jZG4uZWxpZmVzY2llbmNlcy5vcmcvYXJ0aWNsZXMvODE1MDUvZWxpZmUtODE1MDUtdjEucGRmP2Nhbm9uaWNhbFVyaT1odHRwczovL2VsaWZlc2NpZW5jZXMub3JnL2FydGljbGVzLzgxNTA1/elife-81505-v1.pdf?_hash=771fo3bisEGGhiYmdR%2BdPiKymoNeq5NzeBIUdjB0zBE%3D
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Title: eLife
Source Genre: Journal
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Pages: e81505 Volume / Issue: - Sequence Number: - Start / End Page: - Identifier: ISBN: 2050-084X