Regulation of the size and distribution of ectopic neuromuscular junctions in adult skeletal muscle by nerve-derived trophic factor and electrical muscle activity.
Transplanted axons induced multiple, irregularly distributed acetylcholine receptor (AChR) aggregates on muscle fibers at early stages of ectopic neuromuscular junction formation in denervated adult rat soleus muscles. Subsequently, most AChR aggregates disappeared (the losers). A few aggregates survived (the winners) and, as part of the surviving junctions, reached a certain size and spatial separation along the fibers. This elimination of losers and development of winners occurred only in electrically active muscles whether the activity was elicited by intact axons or by electrical muscle stimulation after the axons had been cut early. We conclude that electrical muscle activity regulates the size and distribution of ectopic neuromuscular junctions by acting in conjunction with a nerve-derived priming influence that does not require the continued presence of nerve terminals.
D000818:Animals; D001369:Axons / Q000187:drug effects / Q000502:physiology / Q000637:transplantation; D003714:Denervation; D008297:Male; D018482:Muscle, Skeletal / Q000294:innervation* / Q000502:physiology*; D009407:Nerve Block; D009414:Nerve Growth Factors / Q000502:physiology*; D009431:Neural Conduction / Q000187:drug effects; D009469:Neuromuscular Junction / Q000648:ultrastructure*; D051381:Rats; D017208:Rats, Wistar; D011940:Receptor Aggregation / Q000502:physiology; D011950:Receptors, Cholinergic / Q000378:metabolism; D013569:Synapses / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology