Please use this identifier to cite or link to this item: https://repositorio.ufrn.br/handle/123456789/23214
Title: 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
Authors: Patra, Kalicharan
Lyons, David J.
Bauer, Pavol
Hilscher, Markus M.
Sharma, Swati
Leão, Richardson Naves
Kullander, Klas
Keywords: acetylcholine;peripheral nervous system;SLC10A4;synaptic transmission;vesicular aminergic-associated transporter;vesicular content
Issue Date: 2015
Portuguese 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.
URI: https://repositorio.ufrn.br/jspui/handle/123456789/23214
Appears in Collections:ICe - Artigos publicados em periódicos

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.