Analysis of presynaptic and postsynaptic actions of anesthetics on spinal monosynaptic transmission.

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Publication Type thesis
School or College College of Pharmacy
Department Pharmacology & Toxicology
Author Weakly, James Neal
Title Analysis of presynaptic and postsynaptic actions of anesthetics on spinal monosynaptic transmission.
Date 1968-08
Description The mechanism of the depression of central nervous functions produced by anesthetic agents has been of interest to physiologists, pharmacologist, and physicians for some time. Despite the widespread use of central nervous system depressant, relatively little is known about their effects on nervous tissue at the cellular level, particularly their actions on presynaptic nerve terminals. The present investigation attempts to analyze the effects of three central nervous system depressants, thiopental, pentobarbital, and ether, with the use of the technique of intracellular recording. The monosynaptic pathway in the spinal cord of the cat was selected as the model to be used in this investigation. This selection was made on the basis of the abundance of knowledge that has been accumulated in the past 25 years regarding the physiology of this central pathway, and because the drugs employed in this investigation has been shown to exert effects on the spinal cord by various Neurophysiological and neuro-pharmacological techniques other than intracellular recording. In order to examine the effects of these anesthetics on the presynaptic mechanism(s) responsible for transmitter release, advantage was taken of the fact that transmission of excitation of the spinal monosynaptic pathway is quantal in nature, i.e., transmitter is released as multi-molecular packages of quanta in a manner similar to the transmitter at the neuromuscular junction. In the doses employed, the drugs were observed to block reflex transmission in the monosynaptic pathway. The barbiturates were found to be without effects on parameters attributable to the postsynaptic membrane, i.e., input resistance of the motoneurons membrane, strength-duration relations for the motoneurons, and sensitivity of the subsynaptic membrane to the effects of the transmitter. Thiopental and pentobarbital reduced the amount of transmitter released by a single afferent impulse from a Group la fiber in the muscle nerve. The observed magnitude to the reduction in transmitter release is adequate to explain the reduction in reflex transmission through the pathway. It is concluded that the actions of thiopental and pentobarbital, in the doses employed, are confined to presynaptic nerve terminals and that the depression of reflex transmission in the spinal monosynaptic pathway is the result of a decrease in the statistical probability of transmitter release. Ether also decreased the amount of transmitter released by single afferent impulses, but this does not appear to be the sole factor responsible for the observed decreased in monosynaptic reflex transmission produced by this agent.
Type Text
Publisher University of Utah
Subject Central Nervous System
Subject MESH Anesthetics; Receptors, Neurotransmitter
Dissertation Institution University of Utah
Dissertation Name PhD
Language eng
Relation is Version of Digital reproduction of "Analysis of presynaptic and postsynaptic actions of anesthetics on spinal monosynaptic transmission." Spencer S. Eccles Health Sciences Library. Print version of "Analysis of presynaptic and postsynaptic actions of anesthetics on spinal monosynaptic transmission." available at J. Willard Marriott Library Special Collection. QP6.5 1968 .W4.
Rights Management © James Neal Weakly.
Format Medium application/pdf
Identifier us-etd2,2924
Source Original: University of Utah Spencer S. Eccles Health Sciences Library (no longer available).
Funding/Fellowship USPHS Pharmacology Training Grant No. 5T1 GM 153 and grant no. NB-00872 from the National Institute of Neurological Diseases and Blindness, National Institutes of Health.
ARK ark:/87278/s6640480
Setname ir_etd
Date Created 2012-04-23
Date Modified 2012-04-23
ID 192571
Reference URL