Silencing rapsyn in vivo decreases acetylcholine receptors and augments sodium channels and secondary postsynaptic membrane folding.

Authors: Martinez-Martinez, P  Phernambucq, M  Steinbusch, L  Schaeffer, L  Berrih-Aknin, S  Duimel, H  Frederik, P  Molenaar, P  De Baets, MH  Losen, M 
Citation: Martinez-Martinez P, etal., Neurobiol Dis. 2009 Jul;35(1):14-23. doi: 10.1016/j.nbd.2009.03.008. Epub 2009 Apr 1.
Pubmed: (View Article at PubMed) PMID:19344765
DOI: Full-text: DOI:10.1016/j.nbd.2009.03.008

The receptor-associated protein of the synapse (rapsyn) is required for anchoring and stabilizing the nicotinic acetylcholine receptor (AChR) in the postsynaptic membrane of the neuromuscular junction (NMJ) during development. Here we studied the role of rapsyn in the maintenance of the adult NMJ by reducing rapsyn expression levels with short hairpin RNA (shRNA). Silencing rapsyn led to the average reduction of the protein levels of rapsyn (31% loss) and AChR (36% loss) at the NMJ within 2 weeks, corresponding to previously reported half life of these proteins. On the other hand, the sodium channel protein expression was augmented (66%) in rapsyn-silenced muscles. Unexpectedly, at the ultrastructural level a significant increase in the amount of secondary folds of the postsynaptic membrane in silenced muscles was observed. The neuromuscular transmission in rapsyn-silenced muscles was mildly impaired. The results suggest that the adult NMJ can rapidly produce postsynaptic folds to compensate for AChR and rapsyn loss.

Annotation

Disease Annotations
Gene Ontology Annotations
Objects Annotated

Additional Information

 
CRRD Object Information
CRRD ID: 8549750
Created: 2014-04-03
Species: All species
Last Modified: 2014-04-03
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.