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Time lapse in vivo visualization of developmental stabilization of synaptic receptors at Neuromuscular Junctions

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Yampolsky,  Pessah
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Pacifici,  Pier Giorgio
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Lomb,  Lukas
Department of Biomolecular Mechanisms, Max Planck Institute for Medical Research, Max Planck Society;

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Giese,  Günter
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

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Witzemann,  Veit
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Yampolsky, P., Pacifici, P. G., Lomb, L., Giese, G., Rudolf, R., Roeder, I. V., et al. (2010). Time lapse in vivo visualization of developmental stabilization of synaptic receptors at Neuromuscular Junctions. The Journal of Biological Chemistry, 285(45), 34589-34596. doi:10.1074/jbc.M110.168880.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002C-5F59-7
Abstract
The lifetime of nicotinic acetylcholine receptors (AChRs) in neuromuscular junctions (NMJs) is increased from <1 day to >1 week during early postnatal development. However, the exact timing of AChR stabilization is not known, and its correlation to the concurrent embryonic to adult AChR channel conversion, NMJ remodeling, and neuromuscular diseases is unclear. Using a novel time lapse in vivo imaging technology we show that replacement of the entire receptor population of an individual NMJ occurs end plate-specifically within hours. This makes it possible to follow directly in live animals changing stabilities of end plate receptors. In three different, genetically modified mouse models we demonstrate that the metabolic half-life values of synaptic AChRs increase from a few hours to several days after postnatal day 6. Developmental stabilization is independent of receptor subtype and apparently regulated by an intrinsic muscle-specific maturation program. Myosin Va, an F-actin-dependent motor protein, is also accumulated synaptically during postnatal development and thus could mediate the stabilization of end plate AChR.