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Neural control of the forms of acetylcholinesterase in slow mammalian muscles

Nature volume 321, pages 7274 (01 May 1986) | Download Citation

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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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Author information

Author notes

    • Josephine Lai

    Present address: Laboratory of Neurophysiology, NINCOS, NIH, Bethesda, Maryland 20205, USA.

    • Jolanta Jedrzejczyk

    Permanent address: Department of Histology, Academy of Medicine, Warsaw 02-004, Poland.

    • John A. Pizzey

    Present address: Biophysics Department, KQC Kensington Campus, London W8 7AH, UK.

Affiliations

  1. Department of Biochemistry, Imperial College of Science and Technology, London SW7 2AZ, and MRC Molecular Neurobiology Unit, MRC Centre, Hills Road, Cambridge CB2 2QH, UK

    • Josephine Lai
    • , Jolanta Jedrzejczyk
    • , John A. Pizzey
    • , David Green
    •  & Eric A. Barnard

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DOI

https://doi.org/10.1038/321072a0

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