Abstract
The ‘heavy’, collagen-tailed form of acetylcholinesterase (AChE), having a s20,w° of 16S in mammals, occurs at vertebrate muscle endplates and has been widely regarded as a marker of neuronal influence on muscle in vivo1–5. However, an interesting exception has been described by Bacou et al., in a previous report in Nature6. They found, in a slow-twitch muscle of the rabbit, that after denervation the 16S form of AChE increases markedly, rather than disappearing. Such a phenomenon would modify current concepts of neuromuscular regulation. We report here, however, that this exception is apparent rather than real in terms of endplate AChE regulation.
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Lai, J., Jedrzejczyk, J., Pizzey, J. et al. Neural control of the forms of acetylcholinesterase in slow mammalian muscles. Nature 321, 72–74 (1986). https://doi.org/10.1038/321072a0
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DOI: https://doi.org/10.1038/321072a0
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