Mobility of calcium channels in the presynaptic membrane.

Romy Schneider, Eric Hosy, Johannes Kohl, Julia Klueva, Daniel Choquet, Ulrich Thomas, Andreas Voigt, Martin Heine
Neuron. 2015-05-01; 86(3): 672-679
DOI: 10.1016/j.neuron.2015.03.050

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1. Neuron. 2015 May 6;86(3):672-9. doi: 10.1016/j.neuron.2015.03.050. Epub 2015 Apr
16.

Mobility of calcium channels in the presynaptic membrane.

Schneider R(1), Hosy E(2), Kohl J(3), Klueva J(4), Choquet D(5), Thomas U(6),
Voigt A(7), Heine M(8).

Author information:
(1)Molecular Physiology Group, Leibniz Institute for Neurobiology, D-39118
Magdeburg, Germany.
(2)University of Bordeaux, F-33000 Bordeaux, France; CNRS, Interdisciplinary
Institute for Neuroscience, UMR 5297, F-33000 Bordeaux, France.
(3)Harvard University, Department Molecular and Cellular Biology, Cambridge, MA
02138, USA.
(4)Molecular Physiology Group, Leibniz Institute for Neurobiology, D-39118
Magdeburg, Germany; Presynaptic Plasticity Group, Leibniz Institute for
Neurobiology, D-39118 Magdeburg, Germany.
(5)University of Bordeaux, F-33000 Bordeaux, France; CNRS, Interdisciplinary
Institute for Neuroscience, UMR 5297, F-33000 Bordeaux, France; Bordeaux Imaging
Center, UMS 3420 CNRS, US4 INSERM, University of Bordeaux, F-33000 Bordeaux,
France.
(6)Department Neurochemistry, Leibniz Institute for Neurobiology, D-39118
Magdeburg, Germany.
(7)Otto-von-Guericke-University Magdeburg, Systemverfahrenstechnik,
Universitätsplatz 2, D-39106 Magdeburg, Germany.
(8)Molecular Physiology Group, Leibniz Institute for Neurobiology, D-39118
Magdeburg, Germany. Electronic address: .

Unravelling principles underlying neurotransmitter release are key to understand
neural signaling. Here, we describe how surface mobility of voltage-dependent
calcium channels (VDCCs) modulates release probabilities (P(r)) of synaptic
vesicles (SVs). Coupling distances of 100 nm have been reported for SVs
and VDCCs in different synapses. Tracking individual VDCCs revealed that within
hippocampal synapses, ∼60% of VDCCs are mobile while confined to presynaptic
membrane compartments. Intracellular Ca(2+) chelation decreased VDCC mobility.
Increasing VDCC surface populations by co-expression of the α2δ1 subunit did not
alter channel mobility but led to enlarged active zones (AZs) rather than higher
channel densities. VDCCs thus scale presynaptic scaffolds to maintain local
mobility. We propose that dynamic coupling based on mobile VDCCs supports calcium
domain cooperativity and tunes neurotransmitter release by equalizing Pr for
docked SVs within AZs.

Copyright © 2015 Elsevier Inc. All rights reserved.

DOI: 10.1016/j.neuron.2015.03.050
PMID: 25892305 [Indexed for MEDLINE]


Auteurs Bordeaux Neurocampus