Deutsch
 
Benutzerhandbuch Datenschutzhinweis Impressum Kontakt
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

Electrical activity and postsynapse formation in adult muscle: γ-AChR are not required

MPG-Autoren
/persons/resource/persons123500

Sander,  Andreas
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons123510

Schwarz,  Holger
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons95970

Witzemann,  Veit
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons95089

Sakmann,  Bert
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Hashemolhosseini, S., Moore, C., Landmann, L., Sander, A., Schwarz, H., Witzemann, V., et al. (2000). Electrical activity and postsynapse formation in adult muscle: γ-AChR are not required. Molecular and Cellular Neuroscience, 16(6), 697-707. doi:10.1006/mcne.2000.0911.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0024-322A-7
Zusammenfassung
Skeletal muscle fibers will not accept hyperinnervation by foreign motor axons unless they are paralyzed, suggesting that paralysis makes them receptive to innervation, e.g., by upregulating extrasynaptic expression of small gamma, Greek−AChRs and/or of the agrin receptor MuSK. To examine the involvement of these parameters in paralysis−mediated synapse induction, ectopic expression of agrin, a factor from motor neurons controlling neuromuscular synapse formation, was made dependent on the administration of doxycycline in innervated adult muscle fibers. In response to doxycycline−induced agrin secretion, adult fibers did form ectopic postsynaptic specializations, even when they were electrically active, lacked fetal AChRs, and expressed normal low levels of MuSK. These data demonstrate that paralysis and changes associated with it are not required for agrin−induced postsynapse formation. They suggest that paralyzed muscle induces synapse formation via the release of factors that make motor neurites contact muscle fibers and secrete agrin