English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
  Acetylcholine receptor e-subunit deletion causes muscle weakness and atrophy in juvenile and adult mice

Witzemann, V., Schwarz, H., Koenen, M., Berberich, C., Villarroel, A., Wernig, A., et al. (1996). Acetylcholine receptor e-subunit deletion causes muscle weakness and atrophy in juvenile and adult mice. Proceedings of the National Academy of Sciences of the United States of America, 93, 13286-13291. Retrieved from http://www.pnas.org/cgi/content/abstract/93/23/13286.

Item is

Basic

show hide
Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0024-4DDA-2 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0024-4DEF-3
Genre: Journal Article
Alternative Title : Acetylcholine receptor e-subunit deletion causes muscle weakness and atrophy in juvenile and adult mice

Files

show Files
hide Files
:
PNAS_93_1996_13286.pdf (Any fulltext), 322KB
 
File Permalink:
-
Name:
PNAS_93_1996_13286.pdf
Description:
-
Visibility:
Restricted (Max Planck Institute for Medical Research, MHMF; )
MIME-Type / Checksum:
application/pdf
Technical Metadata:
Copyright Date:
-
Copyright Info:
-
License:
-

Locators

show
hide
Description:
-
Description:
-

Creators

show
hide
 Creators:
Witzemann, Veit1, 2, Author              
Schwarz, Holger2, Author              
Koenen, Michael1, 2, Author              
Berberich, Christoph2, Author              
Villarroel, Alfredo2, Author              
Wernig, A., Author
Brenner, Hans R., Author
Sakmann, Bert2, Author              
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              

Content

show
hide
Free keywords: synapse; homologous recombination; end plate channel; muscle development
 Abstract: In mammalian muscle a postnatal switch in functional properties of neuromuscular transmission occurs when miniature end plate currents become shorter and the conductance and Ca2+ permeability of end plate channels increases. These changes are due to replacement during early neonatal development of the −subunit of the fetal acetylcholine receptor (AChR) by the −subunit. The long−term functional consequences of this switch for neuromuscular transmission and motor behavior of the animal remained elusive. We report that deletion of the −subunit gene caused in homozygous mutant mice the persistence of −subunit gene expression in juvenile and adult animals. Neuromuscular transmission in these animals is based on fetal type AChRs present in the end plate at reduced density. Impaired neuromuscular transmission, progressive muscle weakness, and atrophy caused premature death 2 to 3 months after birth. The results demonstrate that postnatal incorporation into the end plate of −subunit containing AChRs is essential for normal development of skeletal muscle

Details

show
hide
Language(s): eng - English
 Dates: 1996-08-121996-12-11
 Publication Status: Published in print
 Pages: 6
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Degree: -

Event

show

Legal Case

show

Project information

show

Source 1

show
hide
Title: Proceedings of the National Academy of Sciences of the United States of America
  Other : Proc. Natl. Acad. Sci. U. S. A.
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: National Academy of Sciences
Pages: - Volume / Issue: 93 Sequence Number: - Start / End Page: 13286 - 13291 Identifier: ISSN: 0027-8424
CoNE: https://pure.mpg.de/cone/journals/resource/954925427230