Chromophore-Assisted Light Inactivation of the V-ATPase V0c Subunit Inhibits Neurotransmitter Release Downstream of Synaptic Vesicle Acidification

Synaptic vesicle proton V-ATPase is an essential component in synaptic vesicle function. Active acidification of synaptic vesicles, triggered by the V-ATPase, is necessary for neurotransmitter storage. Independently from its proton transport activity, an additional important function of the membrane...

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Published inMolecular neurobiology Vol. 56; no. 5; pp. 3591 - 3602
Main Authors Rama, Sylvain, Boumedine-Guignon, Norah, Sangiardi, Marion, Youssouf, Fahamoe, Maulet, Yves, Lévêque, Christian, Belghazi, Maya, Seagar, Michael, Debanne, Dominique, El Far, Oussama
Format Journal Article
LanguageEnglish
Published New York Springer US 01.05.2019
Springer Nature B.V
Humana Press
Subjects
Acidification
Adenosine triphosphatase
Biomedical and Life Sciences
Biomedicine
Cell Biology
Cellular Biology
Chromophores
H+-transporting ATPase
Inactivation
Life Sciences
Neurobiology
Neurology
Neurosciences
Neurotransmission
Neurotransmitter release
Neurotransmitters
Proteins
Pyramidal cells
SNAP receptors
Synaptic vesicles
GeneGun
V-ATPase
Hippocampal organotypic slice culture
Neurons
Neurotransmission
Chromophore-assisted light inactivation (CALI)
GeneGun Keywords V-ATPase
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Summary:Synaptic vesicle proton V-ATPase is an essential component in synaptic vesicle function. Active acidification of synaptic vesicles, triggered by the V-ATPase, is necessary for neurotransmitter storage. Independently from its proton transport activity, an additional important function of the membrane-embedded sector of the V-ATPase has been uncovered over recent years. Subunits a and c of the membrane sector of this multi-molecular complex have been shown to interact with SNARE proteins and to be involved in modulating neurotransmitter release. The c-subunit interacts with the v-SNARE VAMP2 and facilitates neurotransmission. In this study, we used chromophore-assisted light inactivation and monitored the consequences on neurotransmission on line in CA3 pyramidal neurons. We show that V-ATPase c-subunit V0c is a key element in modulating neurotransmission and that its specific inactivation rapidly inhibited neurotransmission.
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ISSN:0893-7648
1559-1182
DOI:10.1007/s12035-018-1324-1