Neural control of the forms of acetylcholinesterase in slow mammalian muscles

Abstract

The ‘heavy’, collagen-tailed form of acetylcholinesterase (AChE), having a s_20,w^° of 16S in mammals, occurs at vertebrate muscle endplates and has been widely regarded as a marker of neuronal influence on muscle in vivo^1–5. 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.