|
|
| Research article summary (published 13 Sep 2004): |
Nitric oxide synthase activity is required for postsynaptic differentiation of the embryonic neuromuscular junction.
Full Abstract
Agrin, a synapse-organizing protein externalized by motor axons at the neuromuscular junction (NMJ), initiates a signaling cascade in muscle cells leading to aggregation of postsynaptic proteins, including acetylcholine receptors (AChRs). We examined whether nitric oxide synthase (NOS) activity is required for agrin-induced aggregation of postsynaptic AChRs at the embryonic NMJ in vivo and in cultured muscle cells. Inhibition of NOS reduced AChR aggregation at embryonic Xenopus NMJs by 50-90%, whereas overexpression of NOS increased AChR aggregate area 2- to 3-fold at these synapses. NOS inhibitors completely blocked agrin-induced AChR aggregation in cultured embryonic muscle cells. Application of NO donors to muscle cells induced AChR clustering in the absence of agrin. Our results indicate that NOS activity is necessary for postsynaptic differentiation of embryonic NMJs and that NOS is a likely participant in the agrin-MuSK signaling pathway of skeletal muscle cells.
Author information
Author/s: Schwarte, Russell C (RC); Godfrey, Earl W (EW);
Affiliation: Department of Pathology and Anatomy, Eastern Virginia Medical School, Norfolk, VA 23501, USA.
Grants: MH57545 (Agency:NIMH NIH HHS)
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
Journal: Developmental biology (Dev Biol), published in United States. (Language: eng)
Reference: 2004-Sep; vol 273 (issue 2) : pp 276-84
Dates: Created 2004/08/25; Completed 2004/10/06; Revised 2007/11/14;
PMID: 15328012, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
External Links for this article
(including full text providers, if available):
Click Electronic Full-text Provider Links to see options for finding the electronic full text links to this article. Note there may be a subscription or fee required for access to the full text. See our FAQ for information on finding FREE full text articles.
This article may also be located in paper journal collections available in many libraries. Use the Journal and Publication Information above to find the full article.
MeSH headings (categories)
This article was linked to the MESH Headings shown below.
Related articles
These are the highest related articles currently in the database:
- Guanylate cyclase and cyclic GMP-dependent protein kinase regulate agrin signaling at the developing neuromuscular junction.
22 Apr 2007 - Nitric oxide is a downstream mediator of agrin-induced acetylcholine receptor aggregation.
30 Oct 2000 - The Ets transcription factor GABP is required for postsynaptic differentiation in vivo.
13 Aug 2000 - Agrin fragments differentially induce ectopic aggregation of acetylcholine receptors in myotomal muscles of Xenopus embryos.
13 Sep 2000 - Glia cell line-derived neurotrophic factor regulates the distribution of acetylcholine receptors in mouse primary skeletal muscle cells.
30 Dec 2003 - Agrin-induced AChR aggregate formation requires cGMP and aggregate maturation requires activation of cGMP-dependent protein kinase.
30 Jan 2004 - Development of the neuromuscular junction.
2 Jul 2006 - Tyrosine phosphatase regulation of MuSK-dependent acetylcholine receptor clustering.
27 Feb 2005 - Tyrosine phosphorylation of the muscle-specific kinase is exclusively induced by acetylcholine receptor-aggregating agrin fragments.
13 Apr 1998 - An intrinsic distinction in neuromuscular junction assembly and maintenance in different skeletal muscles.
23 Apr 2002
Related Article Map
Legend:
- FREE Full text Article.
- Abstract only.
- Title only. More help.
See a large map of 100+ related articles.