Schwann Cell Development

Stevens B, Ishibashi T, Chen JF, Fields RD (2004) Adenosine an activity-dependent axonal signal regulating MAP kinase and proliferation in developing Schwann cells. Neuron GUa Biol 1 23-34... 

After exposure to 3300 ppm tellurium in the diet for 5 months, rats were markedly impaired in their ability to learn a sequence of behavioral tasks. The administration of 500-3000 ppm tellurium through the diet to pregnant rats resulted in a high incidence of hydrocephalic offspring. Neonatal rats exposed to tellurium via the mother s milk from the day of birth until killing at 7, 14, 21, or 28 days of age developed Schwann cell and myelin degeneration in the sciatic nerves at each age studied. In the central nervous system (CNS), hypomyelination of the optic nerves was demonstrated at 14, 21, and 28 days of age. 

Jessen, K. R. and Mirsky, R. Schwann cell development. In Lazzarini, R. A. (ed.), Myelin Biology and Disorders. Amsterdam Elsevier/Academic Press, 2004, pp. 329-370. 

The neuregulins also act on Schwann cells to stimulate motility and migratory activity. It is postulated that this interaction provides a mechanism by which neurons can influence glial metabolism and behavior, which are important both in development and for peripheral nerve regeneration. 

CNS development are employed for the same purpose in the PNS. PNS microglia-like cells, like microglia in the CNS, are bone-marrow-derived and have a similar repertoire of responses to activation [2], Both oligodendroglia and Schwann cells speed axonal action potential propagation by assembling and maintaining myelin. Capillary endothelial cells linked by tight junctions restrict entry of polar molecules into the PNS, as into the CNS [3],... 

The lepromatous form of leprosy is characterized by loss ofcutaneoussensibility. Hansen sbacillus(Mycobacterium leprae), which proliferates only in environments cooler than the core temperature maintained by most mammals, is capable of infecting Schwann cells in subcutaneous nerves because the basal lamina of these cells contains a-dystroglycan, to which this mycobacterium binds, and because subcutaneous nerves are often cooler than deeper tissues. Lepromatous neuropathy is a common cause of sensory mononeuropathy multiplex in the developing World [16,17]. 

Diphtheria causes a demyelinative neuropathy. Coryne-bacterium diphtheriae colonizes the pharynx or open wounds, and secretes a protein exotoxin. The B subunit of this exotoxin binds to plasma membranes and facilitates entry into cytosol of the A subunit, which catalyzes ADP-ribosylation, and inactivation of an elongation factor required for protein synthesis. Cardiac muscle and Schwann cells are particularly susceptible to this toxin, and hence patients with diphtheria develop cardiomyopathy and demyelinative polyneuropathy [20]. While diphtheria is now uncommon because of childhood immunization against C. diphtheriae, the disruption in preventative medicine programs caused by disintegration of the Soviet Union was followed by a substantial incidence of diphtheritic polyneuropathy in Russia. 

As mentioned previously, myelination is carried out by highly specialized glial cells, oligodendrocytes in the CNS and Schwann cells in the PNS. These cells differentiate from precursor cells of different origin during development the neural crest for Schwann cells, and neural tube for oligodendrocytes. Myelin characteristics differ morphologically in the CNS and in the PNS, and differ also inside the CNS. Thus... 

---