Abstract
The spinal cord is a particularly important part of the central nervous system as a conduit of motor, sensory, and sphincter function. Damage to it causes loss of motor function and, if sufficiently extensive, paralysis. The morphological architecture of spinal cord and its reflex physiology have been described in considerable detail, but the molecular mechanisms involved in the maintenance and loss of functions are relatively little understood. In the past, the biochemical and metabolic properties of spinal cord received little attention in comparison to the effort expended on brain. In the last decade, however, the situation has changed, and a substantial number of studies have been carried out on proteins, enzymes, amino acids, synaptology, and transmitters in the spinal cord. Studies on the metabolism of spinal cord proteins and lipids and of the enzymes mediating their breakdown provide insight into processes of axon and myelin degeneration. Damage to the spinal cord causes structural alterations and accompanying biochemical changes, some of which, e.g., proteinase release and/or activation, have been implicated in the breakdown of the axon-myelin unit. Relatively little is known at the molecular level of injury or diseases of spinal cord, and less concerning the factor(s) regulating spinal cord degeneration and their source. In order to understand spinal cord function, a detailed study of its biochemical properties (i.e. molecular events) is essential, both in the normal situation and in disease.
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