scholarly journals Neuromuscular junctions (NMJs): ultrastructural analysis and nicotinic acetylcholine receptor (nAChR) subunit mRNA expression in offspring subjected to protein restriction throughout pregnancy

2017 ◽  
Vol 98 (2) ◽  
pp. 109-116
Author(s):  
Paula Aiello Tomé de Souza Castro ◽  
Ludimila Canuto Faccioni ◽  
Patrícia Aline Boer ◽  
Robson Francisco Carvalho ◽  
Selma Maria Michelin Matheus ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Neuromuscular Junctions ◽  
Protein Restriction ◽  
Ultrastructural Analysis ◽  
Nachr Subunit ◽  
Nicotinic Acetylcholine ◽  
Subunit Mrna

scholarly journals Nicotinic acetylcholine receptor is internalized via a Rac-dependent, dynamin-independent endocytic pathway

2008 ◽  
Vol 181 (7) ◽  
pp. 1179-1193 ◽  
Author(s):  
Sudha Kumari ◽  
Virginia Borroni ◽  
Ashutosh Chaudhry ◽  
Baron Chanda ◽  
Ramiro Massol ◽  
...  
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Actin Polymerization ◽  
Neuromuscular Junctions ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Endocytic Pathway ◽  
Nicotinic Acetylcholine ◽  
Ovary Cells ◽  
Major Mechanism

Endocytosis of the nicotinic acetylcholine receptor (AChR) is a proposed major mechanism of neuromodulation at neuromuscular junctions and in the pathology of synapses in the central nervous system. We show that binding of the competitive antagonist α-bungarotoxin (αBTX) or antibody-mediated cross-linking induces the internalization of cell surface AChR to late endosomes when expressed heterologously in Chinese hamster ovary cells or endogenously in C2C12 myocytes. Internalization occurs via sequestration of AChR–αBTX complexes in narrow, tubular, surface-connected compartments, which are indicated by differential surface accessibility of fluorescently tagged αBTX–AChR complexes to small and large molecules and real-time total internal reflection fluorescence imaging. Internalization occurs in the absence of clathrin, caveolin, or dynamin but requires actin polymerization. αBTX binding triggers c-Src phosphorylation and subsequently activates the Rho guanosine triphosphatase Rac1. Consequently, inhibition of c-Src kinase activity, Rac1 activity, or actin polymerization inhibits internalization via this unusual endocytic mechanism. This pathway may regulate AChR levels at ligand-gated synapses and in pathological conditions such as the autoimmune disease myasthenia gravis.

scholarly journals Localization of nicotinic acetylcholine receptor alpha-subunit transcripts during myogenesis and motor endplate development in the chick.

1989 ◽  
Vol 108 (3) ◽  
pp. 1025-1037 ◽  
Author(s):  
B Fontaine ◽  
J P Changeux
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Muscle Development ◽  
Neuromuscular Junctions ◽  
Primary Cultures ◽  
Motor Endplate ◽  
Alpha Subunit ◽  
Subunit Gene ◽  
Nicotinic Acetylcholine

In 15-d-old chick latissimi dorsi muscles, the nicotinic acetylcholine receptor (AChR) alpha-subunit mRNA is densely accumulated at the level of subsynaptic nuclei of the motor endplate (Fontaine et al., 1988). In this paper, using in situ hybridization with genomic probes, we further show that the expression of the AChR alpha-subunit gene in the embryo, revealed by the accumulation of mature mRNAs, starts in myotomal cells and persists during the first stages of muscle development in a majority of muscle nuclei. Subsequently, the distribution of AChR alpha-subunit mRNAs becomes restricted to the newly formed motor endplates as neuromuscular junctions develop. To assess the transcriptional activity of individual nuclei in developing muscles, a strictly intronic fragment of the AChR alpha-subunit gene was used to probe in situ the level of unspliced transcripts. AChR alpha-subunit unspliced transcripts accumulate around a large number of sarcoplasmic nuclei at embryonic day 11, but can no longer be detected at their level after embryonic day 16 in the embryo. A similar decrease in the accumulation of AChR alpha-subunit transcripts is observed between day 4 and day 6 in primary cultures of muscle cells. On the other hand, in vivo denervation and in vitro blocking of muscle electrical activity by the sodium channel blocker tetrodotoxin results in an increase in the labeling of muscle nuclei. Yet, only 6% of the muscle nuclei appear labeled by the strictly intronic probes after denervation. The possible significance of such heterogeneity of muscle nuclei during motor endplate formation in AChR gene expression is discussed.

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