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Abnormalities in neuromuscular junction structure and skeletal muscle function in mice lacking the P2X(2) nucleotide receptor

Ryten, M; Koshi, R; Knight, GE; Turmaine, M; Dunn, P; Cockayne, DA; Ford, APW; (2007) Abnormalities in neuromuscular junction structure and skeletal muscle function in mice lacking the P2X(2) nucleotide receptor. NEUROSCIENCE , 148 (3) 700 - 711. 10.1016/j.neuroscience.2007.06.050.

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Abstract

ATP is co-released in significant quantities with acetylcholine from motor neurons at skeletal neuromuscular junctions (NMJ). However, the role of this neurotransmitter in muscle function remains unclear. The P2X(2) ion channel receptor subunit is expressed during development of the skeletal NMJ, but not in adult muscle fibers, although it is re-expressed during muscle fiber regeneration. Using mice deficient for the P2X(2) receptor subunit for ATP (P2X(2)(-/-)), we demonstrate a role for purinergic signaling in NMJ development. Whereas control NMJs Were characterized by precise apposition of pre-synaptic motor nerve terminals and postsynaptic junctional folds rich in acetylcholine receptors (AChRs), NMJs in P2X(2)(-1-) mice were disorganized: misapposition of nerve terminals and post-synaptic AChR expression localization was common; the density of post-synaptic junctional folds was reduced; and there was increased end-plate fragmentation. These changes in NMJ structure were associated with muscle fiber atrophy. In addition there was an increase in the proportion of fast type muscle fibers. These findings demonstrate a role for P2X2 receptor-mediated signaling in NMJ formation and suggest that purinergic signaling may play an as yet largely unrecognized part in synapse formation. (c) 2007 IBRO. Published by Elsevier Ltd. All rights reserved.

Type: Article
Title: Abnormalities in neuromuscular junction structure and skeletal muscle function in mice lacking the P2X(2) nucleotide receptor
DOI: 10.1016/j.neuroscience.2007.06.050
Keywords: ATP, acetylcholine, knockout, mouse, nerve terminal, synapse, EXTRACELLULAR ATP, GUINEA-PIG, CHOLINE-ACETYLTRANSFERASE, ACETYLCHOLINE-RECEPTOR, SYMPATHETIC NEURONS, RAT SOLEUS, EXPRESSION, NEUROTRANSMITTER, ACTIVATION, MYOTUBES
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Neurodegenerative Diseases
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > Div of Biosciences > Neuro, Physiology and Pharmacology
URI: http://discovery.ucl.ac.uk/id/eprint/104434
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