Myelin definition

The transport of information from sensors to the central nervous system and of instructions from the central nervous system to the various organs occurs through electric impulses transported by nerve cells (see Fig. 6.17). These cells consist of a body with star-like projections and a long fibrous tail called an axon. While in some molluscs the whole membrane is in contact with the intercellular liquid, in other animals it is covered with a multiple myeline layer which is interrupted in definite segments (nodes of Ranvier). The Na+,K+-ATPase located in the membrane maintains marked ionic concentration differences in the nerve cell and in the intercellular liquid. For example, the squid axon contains 0.05 MNa+, 0.4 mK+, 0.04-0.1 m Cl-, 0.27 m isethionate anion and 0.075 m aspartic acid anion, while the intercellular liquid contains 0.46 m Na+, 0.01 m K+ and 0.054 m Cl-. 

Histopathological features of white matter lesions include diffuse myelin pallor (sparing the U-fibers, that are supplied by cortical branches), astrocytic gliosis, widening of perivascular spaces, and loss of oligodendrocytes leading to rarefaction, spongiosis, as well as loss of myelin and axons without definite necrosis, which has also been described as incomplete white matter infarction, which may finally... 

A casual examination of the general chemical composition of membranes from mammalian cells reveals that over 90% of their (dry weight) mass is comprised of proteins and phospholipids (in the main). The weight ratio of these two major classes of compounds may vary considerably from one source to another, ranging from 3 1 in myelin to 1 3 in mitochondria. While no definitive figure can be cited for the minimal amount of phospholipid and/or protein required for a membrane structure, it is abundantly clear that any ultimate disclosure of the architecture and behavior of biological membranes... 

The medical school definition of multiple sclerosis (MS) is demyelination within the central nervous system that varies in space and time. The term refers to a disorder in which patches of demyelination develop during exacerbations. In the most common forms of MS, exacerbations are separated by varying periods of time in which the disease does not appear to progress. Whether progressive demyelination without clear periods of remission should be considered a form of MS is a matter of definition, about which clinicians specializing in the care of patients with this disorder have argued. Conventional medical nomenclature classifies as distinct entities a number of disorders of myelin that can mimic MS clinically. These include, for instance, the sometimes devastating demyelination localized to the pons or the demyelination that can follow infectious diseases and/or vaccinations. 

In a recent review article on the anatomy of autism Amaral et al. (2008) point out that in these studies by Casanova and his colleagues, only 14 cases of autism, 9 of which had seizures and at least 10 with mental retardation, have been examined for minicolumn pathology. Consequently, more studies using a greater number of autistic brains with fewer other complications need to be carried out before any definite conclusions can be reached about changes that can only be attributed to autism. It would also be appropriate to examine brains in which the apical dendritic clusters and myelinated axon bundles have been stained to confirm the sizes of the minicolumns as detected in digitized images from autistic brains. 

Little is known of the biosynthesis, breakdown, or role of sulfatides. Two observations seem established the biosynthesis of sulfatides coincides with the appearance of myelin and studies with the aid of a radioactive precursor have established a slow but definite turnover of sulfatides in the adult brain. Consequently, the brain constantly synthesizes and degrades sulfatides. Similar anabolic and catabolic processes are likely to occur in other tissues. 

In summary, lead affects peripheral nerves by damaging Schwann cells and myelin sheaths, by damaging some axons (though not definitely their precursor cells), and by influencing the permeability of blood vessels within nerves. The primary site of damage is not known, nor is it known what effects, if any, may be seen at levels of exposure comparable to those found in the contemporary urban environment. 

Several investigators (Mills and Williams, 1962 Prohaska and Wells, 1974) have observed a marked decrease in the copper content and cytochrome c oxidase activity of neural tissue from copper-deficient animals. Cytochrome c oxidase is a copper-dependent enzyme and the terminal oxidase in the respiratory chain of mitochondria. These facts have led to speculation that the primary lesion in neonatal ataxia is the depression of cytochrome c oxidase, which leads to a diminution of aerobic metabolism and a subsequent decrease in phospholipid and myeline synthesis. Although this hypothesis seems tenable definitive evidence linking the activity of neural cytochrome c oxidase to the production of myelin is lacking. 

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