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WALTER F. Riker, Jr., M.D.

Arch Neurol. 1960;3(5):488-499.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

A pivotal advance in the physiology of neuromuscular transmission was made when Brown et al. (1936) observed for the first time the characteristic action of physostigmine in augmenting the isometric tension developed in response to single maximal nerve volleys. Subsequent analysis by Brown (1937) showed that this effect of physostigmine resulted from the occurrence of repetitive discharges in the muscle, although the motor nerve had been excited but once; these important observations are repictured in Figures 1 and 2. Thus, physostigmine was seen to convert the singletwitch response to a brief asynchronous tetanus and thereby to account for the increased contractile tension. Not only was this the first example of a drug-induced facilitation of neuromuscular transmission but it was also one of the earliest demonstrations of neuromuscular facilitation. Shortly thereafter Eccles et al. (1942) examined this effect of physostigmine in 4.kg. 3.

Fig. 1.—Effect of physostigmine on isometric contractile response . . . [Full Text PDF of this Article]

Author Affiliations
New York

From the Department of Pharmacology, Cornell University Medical College.

Footnotes
Accepted for publication March 9, 1960.

These investigations were supported by a research grant from the National Institute of Neurological Diseases and Blindness, U.S. Public Health Service.

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