Neural Trophism

The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.

Trophism, Neural


the nervous system’s regulatory influence on the structure, chemistry, growth, and development of organs and tissues, achieved by affecting the metabolism. The concept of the trophic function of the nervous system arose early in the 19th century owing to the attempts of clinicians and physiologists to account for the pathological changes occurring in tissues (ulcers, necrosis, and atrophy) upon injury to the nervous system. These changes, known as neurogenic dystrophies, take place when neuroregulation of metabolism in tissues is impaired by injury or chronic irritation of nerve trunks or by injury to the central nervous system, in particular, to the hypothalamus.

In studies on the trophic function of the nervous system made during the 1920’s, I. P. Pavlov maintained that every organ is controlled by the nerves in three ways. Functional control arouses or arrests the activity of organs, vascular control regulates the supply of nutrients by the blood, and trophic control regulates the utilization of nutrients by organs.

Further research on neural trophism was conducted in the USSR by L. A. Orbeli, who advanced a theory of the adapto-trophic function of the sympathetic nervous system, and by A. D. Speranskii, who discovered the pathophysiological mechanisms responsible for tissue dystrophy caused by the action of pathogenic agents on the central and peripheral nervous systems. Numerous clinical observations and experiments suggest that all nerves have a greater or lesser trophic function and that there are few trophic nerves as such; among them are the sympathetic nerves that innervate the heart muscle and fatty tissues. The trophic influence of the sympathetic nerves of the heart is manifested by a stimulation of metabolism in the myocardium. This stimulation accelerates and intensifies the contraction of the automatically functioning heart muscle and accelerates the conduction of stimulation through the heart. The sympathetic trophic nerves of the fatty tissues help mobilize fat reserves when the energy requirements of the body increase.

Loss of the trophic influence of functional nerves may be manifested by atrophy of skeletal muscles lacking in motor innervation. Thus, transection of a motor nerve causes a reduction in the volume of muscle cells, impairs the contractility of the muscle cells, and significantly alters their metabolism. The structure and function of the muscle are gradually restored after the nerve becomes implanted in a muscle. The trophic influence of vascular nerves is clearly apparent in the phenomenon of the adapto-trophic function, discovered by Orbeli and Ginetsinskii. The rapidly progressing impairment of eye tissues after transection of the trigeminal nerve is a classic example of neurogenic dystrophy caused by injury to a sensory nerve.

The mechanisms of neural trophism are still largely obscure. Of great importance are such chemical transmitters of neural excitation as acetylcholine and norepinephrine; other biologically active substances such as histamine, serotonin, and the kinins; and some still unidentified chemical compounds formed in nerve trunks that can affect metabolism in tissues. The trophic function of the nervous system evolved in the animal world as a means of adaptation to changing environmental conditions.


Speranskii, A. D. Elementy postroeniia teorii meditsiny. Moscow-Leningrad, 1935.
Pavlov, I. P. Poln. sobr. soch., 2nd ed., vol. 1. Moscow-Leningrad, 1951.
Orbeli, L. A. Izbr. tr., vol. 2. Moscow, 1962.
Govyrin, V. A. Troficheskaia funktsiia simpaticheskikh nervov serdtsa i skeletnykh myshts. Leningrad, 1967.
Neirogennye distrofia ikhfarmakoterapiia. Leningrad, 1969.
The Denervated Muscle. Edited by E. Gutmann. Prague, 1962.
Guth, L. “’Trophic’ Influences of Nerve on Muscle.” Physiological Reviews, 1968, vol. 48, no. 4.


The Great Soviet Encyclopedia, 3rd Edition (1970-1979). © 2010 The Gale Group, Inc. All rights reserved.
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