scholarly journals Oligodendrocyte Development and Myelin Biogenesis: Parsing Out the Roles of Glycosphingolipids

Physiology ◽  
2009 ◽  
Vol 24 (5) ◽  
pp. 290-297 ◽  
Author(s):  
Nicole Jackman ◽  
Akihiro Ishii ◽  
Rashmi Bansal

The myelin sheath is an extension of the oligoddendrocyte (OL) plasma membrane enriched in lipids that ensheaths the axons of the central and peripheral nervous system. Here, we review the involvement of glycosphingolipids in myelin/OL functions, including the regulation of OL differentiation, lipid raft-mediated trafficking and signaling, and neuronglia interactions.

2010 ◽  
Vol 24 (6) ◽  
pp. 585-592 ◽  
Author(s):  
W. Knoll ◽  
F. Natali ◽  
J. Peters ◽  
R. Nanekar ◽  
C. Wang ◽  
...  

Myelin is a multilamellar membrane which, wrapping the nerve axons, increases the efficiency of nervous signal transmission. Indeed, the molecular components of the myelin sheath interact tightly with each other and molecules on the axonal surface to drive myelination, to keep both myelin and the axon intact, and to transduce signals from myelin to the axon and vice versa. Myelin is strongly affected in human demyelinating diseases in both the central and peripheral nervous system (CNS and PNS, respectively). Despite the presence of a well-defined set of myelin-specific proteins, little is known about the structure and the dynamics of these proteins, their interactions with the membrane and their influence on myelin stability. We present here the first neutron scattering results on the dynamics of the myelin sheath in PNS and of the interaction between its constituents. Specifically, the human P2 protein is shown to stabilize the lipid membrane upon binding to it.


2018 ◽  
Vol 215 (3) ◽  
pp. 941-961 ◽  
Author(s):  
Sarah D. Ackerman ◽  
Rong Luo ◽  
Yannick Poitelon ◽  
Amit Mogha ◽  
Breanne L. Harty ◽  
...  

Myelin is a multilamellar sheath generated by specialized glia called Schwann cells (SCs) in the peripheral nervous system (PNS), which serves to protect and insulate axons for rapid neuronal signaling. In zebrafish and rodent models, we identify GPR56/ADGRG1 as a conserved regulator of PNS development and health. We demonstrate that, during SC development, GPR56-dependent RhoA signaling promotes timely radial sorting of axons. In the mature PNS, GPR56 is localized to distinct SC cytoplasmic domains, is required to establish proper myelin thickness, and facilitates organization of the myelin sheath. Furthermore, we define plectin—a scaffolding protein previously linked to SC domain organization, myelin maintenance, and a series of disorders termed “plectinopathies”—as a novel interacting partner of GPR56. Finally, we show that Gpr56 mutants develop progressive neuropathy-like symptoms, suggesting an underlying mechanism for peripheral defects in some human patients with GPR56 mutations. In sum, we define Gpr56 as a new regulator in the development and maintenance of peripheral myelin.


1991 ◽  
Vol 39 (12) ◽  
pp. 1645-1658 ◽  
Author(s):  
K Maggio ◽  
A Watrin ◽  
E Keicher ◽  
G Nicaise ◽  
M L Hernandez-Nicaise

The localization of Ca(2+)- and Mg(2+)-ATPases was determined in Aplysia central and peripheral nervous system, using an electron microscopic cytochemical method. The enzyme activity appeared localized to the membrane of glial granules (gliagrana), particularly in the peripheral nervous system of the esophagus, and on the plasma membrane of central glial cells adjacent to neuronal cell bodies. No calcium- and/or magnesium-ATPase activity was detectable on the plasma membrane of glial cells surrounding nerve axons in the pleuro-visceral connectives. These findings are discussed along two main lines: (a) the calcium-ATPase of the gliagrana coincides with a high intragranular calcium and/or proton concentration; and (b) the presence of a calcium-ATPase activity at the glio-neuronal interface around the neuronal cell bodies coincides with the use of calcium ions as charge carriers of the action potential, and its absence at the level of the axon with the concurrent functional use of sodium ions.


Author(s):  
M. A. Hayat

Potassium permanganate has been successfully employed to study membranous structures such as endoplasmic reticulum, Golgi, plastids, plasma membrane and myelin sheath. Since KMnO4 is a strong oxidizing agent, deposition of manganese or its oxides account for some of the observed contrast in the lipoprotein membranes, but a good deal of it is due to the removal of background proteins either by dehydration agents or by volatalization under the electron beam. Tissues fixed with KMnO4 exhibit somewhat granular structure because of the deposition of large clusters of stain molecules. The gross arrangement of membranes can also be modified. Since the aim of a good fixation technique is to preserve satisfactorily the cell as a whole and not the best preservation of only a small part of it, a combination of a mixture of glutaraldehyde and acrolein to obtain general preservation and KMnO4 to enhance contrast was employed to fix plant embryos, green algae and fungi.


Author(s):  
S.S. Spicer ◽  
B.A. Schulte

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.


2000 ◽  
Vol 5 (2) ◽  
pp. 3-3
Author(s):  
Christopher R. Brigham ◽  
James B. Talmage

Abstract Lesions of the peripheral nervous system (PNS), whether due to injury or illness, commonly result in residual symptoms and signs and, hence, permanent impairment. The AMA Guides to the Evaluation of Permanent Impairment (AMA Guides) describes procedures for rating upper extremity neural deficits in Chapter 3, The Musculoskeletal System, section 3.1k; Chapter 4, The Nervous System, section 4.4 provides additional information and an example. The AMA Guides also divides PNS deficits into sensory and motor and includes pain within the former. The impairment estimates take into account typical manifestations such as limited motion, atrophy, and reflex, trophic, and vasomotor deficits. Lesions of the peripheral nervous system may result in diminished sensation (anesthesia or hypesthesia), abnormal sensation (dysesthesia or paresthesia), or increased sensation (hyperesthesia). Lesions of motor nerves can result in weakness or paralysis of the muscles innervated. Spinal nerve deficits are identified by sensory loss or pain in the dermatome or weakness in the myotome supplied. The steps in estimating brachial plexus impairment are similar to those for spinal and peripheral nerves. Evaluators should take care not to rate the same impairment twice, eg, rating weakness resulting from a peripheral nerve injury and the joss of joint motion due to that weakness.


2004 ◽  
Author(s):  
G. Galietta ◽  
A. Capasso ◽  
A. Fortuna ◽  
F. Fabi ◽  
P. Del Basso ◽  
...  

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