Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Exercise modulates synaptic acetylcholinesterase at neuromuscular junctions.

Authors: Blotnick, E  Anglister, L 
Citation: Blotnick E and Anglister L, Neuroscience. 2016 Apr 5;319:221-32. doi: 10.1016/j.neuroscience.2016.01.044. Epub 2016 Jan 25.
Pubmed: (View Article at PubMed) PMID:26820598
DOI: Full-text: DOI:10.1016/j.neuroscience.2016.01.044

Acetylcholinesterase plays a major role in neuromuscular transmission and is regulated by neuromuscular activity. Since fast-twitch motor units are recruited with increased motor demand, we examined acetylcholinesterase regulation in rat leg muscles following treadmill training. Total acetylcholinesterase and specifically the membrane-bound tetramer increased in exercised fast-, but not slow-twitch muscles, while other isoforms remained unchanged. Synaptic acetylcholinesterase increased markedly in neuromuscular junctions of trained fibers, without concomitant changes in synaptic acetylcholine receptor, thus elevating synaptic acetylcholinesterase/receptor ratios. Electron microscopy showed that acetylcholinesterase increased in postjunctional folds and primary cleft, where it was added adjacent to the postsynaptic muscle membrane. Thus, although the primary acetylcholinesterase at the neuromuscular junction is the collagen-tailed asymmetric isoform associated with synaptic basal lamina, physiological demands such as strenuous exercise, or potentially pathological conditions, can selectively recruit the membrane-bound acetylcholinesterase tetramer to the synapse for optimal synaptic transmission.

Annotation

Gene Ontology Annotations
Objects Annotated

Additional Information

 
RGD Object Information
RGD ID: 12050110
Created: 2017-01-21
Species: All species
Last Modified: 2017-01-21
Status: ACTIVE



NHLBI Logo

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