JPET xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
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 Longo, V. G.
Right arrow Articles by Unna, K. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Longo, V. G.
Right arrow Articles by Unna, K. R.
Journal of Pharmacology And Experimental Therapeutics, Vol. 129, Issue 1, 61-68, 1960
Copyright © 1960 by American Society for Pharmacology and Experimental Therapeutics


A PHARMACOLOGICAL STUDY ON THE RENSHAW CELL

V. G. Longo 1, W. R. Martin 2, and K. R. Unna 3

1 Istituto Superiore di Sanitá, Rome, Italy
2 National Insitute of Mental Health, Addiction Tesearch Center, U. S. Public Health Service Hospital, Lexington, Ky.
3 Department of Pharmacology, University of Illinois College of Medicine, Chicago, Illinois

The effects of varying strengths of stimulation, physostigmine, dihydro-beta-erythroidine and mephenesin on the frequency of spike activity of the Renshaw cell have been investigated. In agreement with Renshaw (1946) and Eccles (1954), it was found that increasing strength of stimulation produced an increase in frequency and duration of discharge of the Renshaw cell, and that physostigmine prolonged the duration of the Renshaw burst. However, measurements of the relationship between the time course of the Renshaw burst and stimulus strength yielded data inconsistent with the hypothesis that the duration of the burst is determined solely by the rate of hydrolysis of acetylchohine. The effect of physostigmine in prolonging the Renshaw burst can be explained on the basis that, in the presence of a reduced concentration of effective esterase, the rate of hydrolysis of ACh would proceed at a slower rate and the concentration of ACh available for combination with effector receptors would be increased.

Dihydro-beta-erythroidine, as Eccles et al. (1954, 1956a) have previously reported, attenuated the duration of the Renshaw burst. In addition, it decreased the frequency of the burst during the first 5 milliseconds. Mephenesin produced a modest depression of the Renshaw burst that was probably of the same order of magnitude as that observed with pentobarbital by Eccles et al. (1956a).

Submitted on October 26, 1959







Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
 Molecular Interventions Drug Metabolism and Disposition

Copyright © 1960 by the American Society for Pharmacology and Experimental Therapeutics.