Reaction of sensory spinal ganglion neurons to transection of their peripheral and central processes

Abstract

The principal clinical consequences of spinal cord trauma in man are associated with the level of damage to the fibers in the spinal cord, and with the dynamics of the degenerative and recuperative processes. Model experiments in animals have made possible the solution of applied and theoretical problems of the study of the mechanisms of the reparative processes in the nervous system. Despite numerous investigations devoted to the changes in nerve cells in the presence of damage to their processes [4, 10, 12, 15], at the present time there is no unified opinion regarding the character and outcome of the reaction of sensory neurons to spinal cord trauma. A number of authors have observed the retrograde degeneration of sensory neurons of the spinal cord ganglion (SCG) and their death only in the presence of transection of the peripheral processes [6, 10, 11, 16, 17], often not at all examining their reaction in the case of the transection of the central processes. However, there exists a no less numerous group of studies in which the degeneration of sensory neurons in response to trauma to their central processes has been demonstrated [3, 5, 8]. The contradictory character of these data, as well as some difficulty in comparing them, is associated with the varied character of the experimental influence (transcompression and transection), with the varied level of the injury (transection of the spinal cord and the crushing of the root), with the various periods of analysis of the material, and with the use of young and adult animals. Only isolated studies have been devoted to the investigation of their central and peripheral processes [2, 14], but the absence of statistical data and of the results of a quantitative analysis of the neurons make the interpretation of the data difficult. The purpose of the present study was the investigation of the dynamics of the reaction of SCG sensory neurons in the presence of injury to their peripheral and central processes in model experiments involving hemisection of this ganglion.