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A role for solute carrier family 10 member 4, or vesicular aminergic‐associated transporter, in structural remodelling and transmitter release at the mouse neuromuscular junction

A role for solute carrier family 10 member 4, or vesicular aminergic‐associated transporter, in... The solute carrier and presynaptic vesicle protein solute carrier family 10 member 4, or vesicular aminergic‐associated transporter (VAAT), was recently proven to have a modulatory role in central cholinergic signalling. It is currently unknown whether VAAT also affects peripheral cholinergic synapses. Here we demonstrated a regulatory role for the presynaptic vesicle protein VAAT in neuromuscular junction (NMJ) development and function. NMJs lacking VAAT had fewer branch points, whereas endplates showed an increased number of islands. Whereas the amplitude of spontaneous miniature endplate potentials in VAAT‐deficient NMJs was decreased, the amplitude of evoked endplate potentials and the size of the readily releasable pool of vesicles were both increased. Moreover, VAAT‐deficient NMJs displayed aberrant short‐term synaptic plasticity with enhanced synaptic depression in response to high‐frequency stimulation. Finally, the transcript levels of cholinergic receptor subunits in VAAT‐deficient muscles were increased, indicating a compensatory postsynaptic sensitization. Our results suggested that VAAT modulates NMJ transmission efficiency and, as such, may represent a novel target for treatment of disorders affecting motor neurons. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Neuroscience Wiley

A role for solute carrier family 10 member 4, or vesicular aminergic‐associated transporter, in structural remodelling and transmitter release at the mouse neuromuscular junction

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References (45)

Publisher
Wiley
Copyright
Copyright © 2015 Federation of European Neuroscience Societies and John Wiley & Sons Ltd
ISSN
0953-816X
eISSN
1460-9568
DOI
10.1111/ejn.12790
pmid
25410831
Publisher site
See Article on Publisher Site

Abstract

The solute carrier and presynaptic vesicle protein solute carrier family 10 member 4, or vesicular aminergic‐associated transporter (VAAT), was recently proven to have a modulatory role in central cholinergic signalling. It is currently unknown whether VAAT also affects peripheral cholinergic synapses. Here we demonstrated a regulatory role for the presynaptic vesicle protein VAAT in neuromuscular junction (NMJ) development and function. NMJs lacking VAAT had fewer branch points, whereas endplates showed an increased number of islands. Whereas the amplitude of spontaneous miniature endplate potentials in VAAT‐deficient NMJs was decreased, the amplitude of evoked endplate potentials and the size of the readily releasable pool of vesicles were both increased. Moreover, VAAT‐deficient NMJs displayed aberrant short‐term synaptic plasticity with enhanced synaptic depression in response to high‐frequency stimulation. Finally, the transcript levels of cholinergic receptor subunits in VAAT‐deficient muscles were increased, indicating a compensatory postsynaptic sensitization. Our results suggested that VAAT modulates NMJ transmission efficiency and, as such, may represent a novel target for treatment of disorders affecting motor neurons.

Journal

European Journal of NeuroscienceWiley

Published: Feb 1, 2015

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