AJP Legacy Add DOIs to your references at manuscript stage!
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol 184: 209-219, 1955;
0002-9513/55 $5.00
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wright, E. B.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Wright, E. B.

Action of Physostigmine (Eserine) Sulfate on Peripheral Nerve

Ernest B. Wright 1

1 From the University of Rochester School of Medicine and Dentistry, Rochester, New York

The effect of eserine (physostigmine) sulfate on frog and rabbit nerve has been studied. Concentrations ranging from 0.005–0.08 m caused: a) a reversible block of conduction in from 50–120 minutes in frog nerve, 20–40 minutes in rabbit nerve; b) the threshold (rheobase) to rise to three times normal value in frog nerve and up to five times normal value in rabbit nerve; c) No change in the value of the excitability constant k; d) The refractory periods to be greatly lengthened. Absolute periods of 10 msec., relative periods of 50 msec were obtained; e) a 60% reduction in the conduction velocity; f) a slight depolarization of less than 2 mv.

A constant anodal voltage applied along 3 cm length of nerve partially relieves the eserine blocking action, cathodal voltage enhances the drug action.

Nerve conduction is blocked much quicker with continuous stimulation, due to the lengthening of the refractory period.

Following a brief interruption of continuous stimulation, a second or less, an action potential can be elicited again. This spike is almost identical with the action potential of a nonstimulated nerve subjected to eserine for the same period of time.

The blocking action cannot be due to acetylcholine accumulation by the anticholinesterase activity of eserine, but rather is due to the inactivation of the sodium mechanism by the drug. Eserinized nerve loses some sodium quickly, large amounts of potassium more slowly.

Submitted on August 8, 1955







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 1955 by the American Physiological Society.