Abstract
STRONG evidence indicates that muscle activity represses the synthesis of extra-synaptic acetylcholine receptor (AChR) in vertebrate skeletal muscle—(1) electrical stimulation of adult denervated muscle prevents the development of acetylcholine supersensitivity1,2 and blocks the incorporation of radiolabelled amino acids into the AChR protein3; (2) in vitro, electrical stimulation of embryonic myotubes also causes a decrease in the rate of AChR synthesis; moreover, the abolition of the spontaneous contraction of the myotubes by tetrodotoxin (TTX) leads to an increase of newly synthesised receptor molecules4–6; (3) chronic paralysis of the neuromuscular junction by cholinergic antagonists increases the synthesis of extrasynaptic AChR in adult and embryonic myofibre7–9. In addition, it has been claimed that ‘trophic’ factors other than the neurotransmitter acetylcholine10–14 regulate the level of extrasynaptic AChR. We show here that the synthesis of AChR in cultured embryonic myotubes is modified by cyclic nucleotide derivatives, and we suggest that cyclic nucleotides may serve as intracellular signals15 in both activity-mediated and neurotrophic control of extrasynaptic AChR synthesis.
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BETZ, H., CHANGEUX, JP. Regulation of muscle acetylcoline receptor synthesis in vitro by cyclic nucleotide derivatives. Nature 278, 749–752 (1979). https://doi.org/10.1038/278749a0
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DOI: https://doi.org/10.1038/278749a0
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