English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

The neuromuscular junction: Selective remodeling of synaptic regulators at the nerve/muscle interface

MPS-Authors
/persons/resource/persons95970

Witzemann,  Veit
Working Group Witzemann / Koenen, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons92478

Chevessier,  Frédéric
Working Group Witzemann / Koenen, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons94653

Pacifici,  Pier Giorgio
Working Group Witzemann / Koenen, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons96022

Yampolsky,  Pessah
Working Group Witzemann / Koenen, Max Planck Institute for Medical Research, Max Planck Society;

Fulltext (public)
There are no public fulltexts available
Supplementary Material (public)
There is no public supplementary material available
Citation

Witzemann, V., Chevessier, F., Pacifici, P. G., & Yampolsky, P. (2013). The neuromuscular junction: Selective remodeling of synaptic regulators at the nerve/muscle interface. Mechanisms of Development, 130(6-8), 402-411. doi:10.1016/j.mod.2012.09.004.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0019-8F08-6
Abstract
The peripheral synapses between motoneurons and skeletal muscle fibers, the neuromuscular junctions, are ideal to investigate the general principles of synaptogenesis that depend on the interaction of activity-dependent and activity-independent signals. Much has been learned from gene “knock out” mouse models that helped to identify major synaptic regulators. The “knock out” approach, however, may not distinguish between changes arising from the disruption of molecular signaling pathways and changes caused by the absence of synaptic transmission. To circumvent these problems, postsynaptic activity was modulated in mouse models by specifically targeting endplate receptors or the activity of synaptic regulators such as MuSK. Both regulators have multiple functions and acetylcholine receptors are not just signal transducers but regulate the localization and architecture of endplates. The results show that detailed analysis of mouse models will help to understand the complexity in mechanisms that regulate synaptic remodeling