Peripheral nervous system Schwann cells

Schwann s ceDs cells that produce myelin in the peripheral nervous system. These cells are located between the axon and axon terminal of neurons and create the myelin sheath which aides in insulating axons and in increasing impulse speeds as they are propagated through the neuron (allowing for salutatory conduction). 

The Schwann cell is the myelin-producing cell of the peripheral nervous system 16... 

The Schwann cell is the myelin-producing cell of the peripheral nervous system. When axons leave the CNS, they lose their neuroglial interrelationships and traverse a short transitional zone where they are invested by an astroglial sheath enclosed in the basal lamina of the glia limitans. The basal lamina then becomes continuous with... 

FIGURE 4-10 Myelin formation in the peripheral nervous system. (A) The Schwann cell has surrounded the axon but the external surfaces of the plasma membrane have not yet fused in the mesaxon. (B) The mesaxon has fused into a five-layered structure and spiraled once around the axon. (C) A few layers of myelin have formed but are not completely compacted. Note the cytoplasm trapped in zones where the cytoplasmic membrane surfaces have not yet fused. (D) Compact myelin showing only a few layers for the sake of clarity. Note that Schwann cell cytoplasm forms a ring both inside and outside of the sheath. (Adapted with permission from Norton, W. T. The myelin sheath. In E. S. Goldensohn and S. H. Appel (eds), Scientific Approaches to Clinical Neurology. Philadelphia Lea Febiger, 1977, pp. 259-298.)... 

The molecular and cellular events during Wallerian degeneration in the peripheral nervous system transform the damaged nerve into an environment that supports regeneration 518 Both Schwann cells and basal lamina are required for axonal regeneration... 

Stoll, G., Griffin, J. W., Li, C. Y. and Trapp, B. D. Wallerian degeneration in the peripheral nervous system participation of both Schwann cells and macrophages in myelin degradation./. Neurocytol. 18 671-683,1989. 

Oligodendrocytes are present in the CNS as well and wrap around axons to form a myelin sheath. Myelin wraps into concentric layers that spiral around the axon. Gaps in the oligodendrocytes are the nodes of Ranvier, where the membrane maintains contact with extracellular fluid. The nodes serve to propagate the action potential in myelinated axons. Schwann cells perform an analogous function, myelinating axons in the peripheral nervous system. Not all neurons are myelinated, but myelination increases the metabolic efficiency of action potentials. Demyelination of neurons produces deficits in neuronal conduction, as is seen in multiple sclerosis. 

Type XXVIII collagen belongs to the class of VWA domain-containing proteins. The primary structure is similar to type VI collagen. It is mainly a component of the basement membranes around Schwann cells in the peripheral nervous system. ... 

Fig. 1. Peripheral and central mechanism of neuropathic pain caused by vincristine. The upper diagram shows the effect of vincristine on the peripheral nervous system (comprising Schwann cells and the dorsal root ganglion (DRG)) and the involvement of interleukin (IL)-6 derived from infiltrating macrophages in neuropathic pain caused by vincristine. The lower diagram shows the effect of vincristine on the central nervous system, and the involvement of tumor necrosis factor-a (TNF-a) derived from activated microglia and astrocytes in neuropathic pain caused by vincristine.

Polyneuropathy with both sensory and motor involvement is much more common among cancer patients than pure SN [83, 110, 111]. SCLC is the most common associated tumor, although other solid tumors may be found [112]. Sensory-motor neuropathy is a quite common paraneoplastic feature in patients with onconeural antibodies, especially Hu and CRMP-5 antibodies. The CRMP-5 antibody is particularly associated with SCLC and thymoma [30]. The CRMP-5 antibody binds to oligodendrocytes as well as to neurons in specific brain regions and the retina and Schwann cells of the peripheral nervous system. In accordance with this, the clinical characteristics are heterogeneous. Many patients exhibit mixed axonal and demye-linating sensory-motor neuropathy, optic neuritis, or cerebellar dysfynction [85, 113], as well as extrapyramidal symptoms (Chapter 5.3). 

P2 is a component of myelin from the peripheral nervous system. It is localized on the cytoplasmic side of Schwann cells where it behaves as peripheral membrane protein, although a small amount is found in the cytoplasm (Trapp et al., 1984). Like the other iLBPs, the exact biochemical role of P2 is unknown. Its cellular localization and its ability to bind different fatty acids and retinoids (Uyemura et al., 1984) suggest that it may function in fatty acid trafficking. It would therefore play a major role in the movement of fatty acids between the site of uptake and that of esterification during the massive phospholipid synthesis phase of myelinating Schwann cells. 

Conduction velocity of an action potential can be increased dramatically by the presence of myelin, a fatty sheath that surrounds the axon and that is interrupted into gaps every millimeter or so at the nodes of Ranvier. Myelin is elaborated by Schwann cells in the peripheral nervous system and by oligodendrocytes in the central nervous system (the biochemistry of myelin will be discussed later in the article). The presence of myelin will dramatically alter the mode and velocity of conduction of the action potential in the axon. As in unmyelinated nerves, the action potential is still transmitted from one section of the axon to another by the presence of local circuit currents. However, the fatty sheath of myelin has poor conduction properties and therefore acts as an insulator. Hence, the local circuit currents jump from one gap to another at the nodes of Ranvier and the rate of conduction is enhanced as local circuit currents travel faster than the action potential itself This process of discontinuous conduction is known as saltatory conduction. Numerous diseases involving myelin deficiency have been described clinically. As one might predict, demyelinating diseases have profound effects on neuronal conduction and on the well-being of the patient. A few of these conditions will be described briefly in the upcoming section on myelin biochemistry. 

Ultrastructural localizations of laminin have also been carried out at the electron microscope level during development and regeneration of the mouse sciatic nerve (Kuecherer-Ehret et al., 1990), in order to ascertain the distribution of laminin during elaboration of the peripheral nervous system. Laminin distribution is not restricted to the BL secreted by the Schwann cells, but is also found in direct contact with developing axons, as well as on the surface of the Schwann cells such a distribution reinforces the idea that laminin is involved in the outgrowth process in vivo. 

Because cholesterol and phospholipid synthesis is likely to be necessary for the maintenance of the integrity of the structural lipoproteins in nervous tissue, especially in the Schwann cells and the oligodendrocytes, and also because cholesterol and fatty acid synthesis is decreased in livers of diabetics, cholesterol and fatty acid synthesis has been measured in the central and peripheral nervous tissue of animals made diabetic with alloxan. The synthesis of both compounds is decreased in diabetic animals in the central but not in the peripheral nervous system. Whether the extension of such studies will someday lead to the elucidation of the pathogenesis of diabetic neuropathy remains to be seen. 

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