Clustered Ca2+ Channels Are Blocked by Synaptic Vesicle Proton Release at Mammalian Auditory Ribbon Synapses

Philippe F.Y. Vincent, Soyoun Cho, Margot Tertrais, Yohan Bouleau, Henrique von Gersdorff, Didier Dulon
Cell Reports. 2018-12-01; 25(12): 3451-3464.e3
DOI: 10.1016/j.celrep.2018.11.072

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1. Cell Rep. 2018 Dec 18;25(12):3451-3464.e3. doi: 10.1016/j.celrep.2018.11.072.

Clustered Ca2+ Channels Are Blocked by Synaptic Vesicle Proton Release at
Mammalian Auditory Ribbon Synapses.

Vincent PFY(1), Cho S(2), Tertrais M(1), Bouleau Y(1), von Gersdorff H(3), Dulon
D(4).

Author information:
(1)Université de Bordeaux, Bordeaux Neurocampus, Equipe Neurophysiologie de la
Synapse Auditive, Inserm U1120, 33076 Bordeaux, France.
(2)Center for Sensory Neuroscience, Boys Town National Research Hospital, Omaha,
NE 68131, USA; The Vollum Institute, Oregon Health and Science University,
Portland, OR 97239, USA.
(3)The Vollum Institute, Oregon Health and Science University, Portland, OR
97239, USA. Electronic address: .
(4)Université de Bordeaux, Bordeaux Neurocampus, Equipe Neurophysiologie de la
Synapse Auditive, Inserm U1120, 33076 Bordeaux, France. Electronic address:
.

A Ca2+ current transient block (ICaTB) by protons occurs at some ribbon-type
synapses after exocytosis, but this has not been observed at mammalian hair
cells. Here we show that a robust ICaTB occurs at post-hearing mouse and gerbil
inner hair cell (IHC) synapses, but not in immature IHC synapses, which contain
non-compact active zones, where Ca2+ channels are loosely coupled to the release
sites. Unlike ICaTB at other ribbon synapses, ICaTB in mammalian IHCs displays a
surprising multi-peak structure that mirrors the EPSCs seen in paired recordings.
Desynchronizing vesicular release with intracellular BAPTA or by deleting
otoferlin, the Ca2+ sensor for exocytosis, greatly reduces ICaTB, whereas
enhancing release synchronization by raising Ca2+ influx or temperature increases
ICaTB. This suggests that ICaTB is produced by fast multivesicular proton-release
events. We propose that ICaTB may function as a submillisecond feedback mechanism
contributing to the auditory nerve’s fast spike adaptation during sound
stimulation.

Copyright © 2018. Published by Elsevier Inc.

DOI: 10.1016/j.celrep.2018.11.072
PMID: 30566869

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