IT was recently shown by Brown et al. [1936] that a very small dose of acetylcholine, injected directly into the empty blood vessels of a normal mammalian muscle, causes a quick contraction of the muscle, resembling a rather slow, single twitch. This contraction has now been shown by electrical records [Brown, 1936] to be a short, asynchronous tetanus, and not a contracture. It was also shown that, under suitable conditions, a small dose of eserine greatly potentiates the response of a mammalian muscle to a single maximal volley of impulses in its motor nerve, and that this potentiated " twitch " is also due to a repetitive response of the muscle, causing a brief, waning tetanus. It was suggested that these observations support the conception of a chemical transmission of excitation from motor nerve to voluntary muscle, by the release of acetylcholine at the nerve endings. The object of our experiments has been to extend these observations, and to test further their bearing on this theory.The longer known effect of acetylcholine on denervated mammalian muscle, producing a response which is largely, at least, a contracture, was shown by Dale & Gass er [1926] to belong to that group of its actions which resemble those of nicotine [Dale, 1914]. It was of interest to know whether acetylcholine produced the rapid response of normal mammalian muscle in virtue of the same nicotine-like activity. We have therefore tested for this effect a number of choline esters and other substances having a "nicotine" action, and one choline ester of which the action is almost entirely of the "muscarine" type. Brown et al. attributed the potentiating action of eserine to inhibition of cholinesterase at the motor nerve endings. We have accordingly examined a series of synthetic I Fellow of the Rockefeller Foundation.
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