Some Aspects of Remyelination after Demyelination Produced by the Intraneural Injection of Lysophosphatidyl Choline

1973 ◽  
Vol 13 (2) ◽  
pp. 461-477
Author(s):  
SUSAN M. HALL

The morphology of remyelination following demyelination induced by the intraneural injection of lysophosphatidyl choline, LPC, has been examined in the mouse sciatic nerve, at periods up to 240 days post-injection. It was found that, in many fibres, the process resembled primary myelinogenesis. There was a moderate Schwann cell proliferation; those Schwann cells not involved in remyelination remained closely associated with the remyelinating Schwann cell/axon unit, within a common basal lamina tube. Numerous small axons, considered to be sprouts from the remyelinating axon, were observed lying in contact with the ‘supernumerary Schwann cells’. In a small population of fibres, however, atypical morphological features were consistently seen: (i) multiple mesaxons, indicating probable remyelination by tunication; (ii) paranodal reorganization in the junctional zone; (iii) the formation of internodal ‘pseudonodes’, which subsequently underwent transition into incisures of Schmidt-Lanterman. These structures are discussed in terms of the re-establishment of the Schwann cell/axon relationship.

1967 ◽  
Vol 34 (3) ◽  
pp. 735-743 ◽  
Author(s):  
A. K. Asbury

Proliferation of Schwann cells in neonatal mouse sciatic nerve was studied radioautographically in 1-µ glycol methacrylate sections. 28 mice were injected with thymidine-3H, 4 µc/g, 48 hr after birth, and were killed serially over the next 4 days. For the cell cycle following injection, the generation time was approximately 24 hr as determined by grain-count halving data; the duration of synthesis phase was 8 hr as determined from a curve constructed from the per cent of mitotic figures containing label; and the labeling index was 9% at 2 hr after injection. With these estimates, the per cent of Schwann cells proliferating was calculated to be 27%. In addition, roughly 25% of dividing cells appeared to cease division during the cell cycle under study. The relationship of these findings to other events during maturation of nerve is discussed.


1987 ◽  
Vol 104 (3) ◽  
pp. 655-660 ◽  
Author(s):  
J E Yoshino ◽  
P W Mason ◽  
G H DeVries

Schwann cell proliferation induced by a myelin-enriched fraction was examined in vitro. Although nearly all the Schwann cells contained material that was recognized by antisera to myelin basic protein after 24 h, only 1% of the cells were synthesizing DNA. 72 h after the addition of the mitogen a maximum of 10% of the cells incorporated [3H]thymidine. If the cultures were treated with the myelin-enriched fraction for 24 h and then washed, the number of proliferating Schwann cells decreased by 75% when compared with those cells that were incubated with the mitogen continuously. When Schwann cells were labeled with [14C]thymidine followed by a pulse of [3H]thymidine 24 h later, every Schwann cell labeled with [3H]thymidine was also labeled with [14C]thymidine. Although almost every Schwann cell can metabolize the myelin membranes within 24 h of exposure, a small population of cell initially utilizes the myelin as a mitogen, and this population continues to divide only if myelin is present in the extracellular media. The percentage of the Schwann cells that initially recognize the myelin-enriched fraction as a mitogen is dependent upon the age of the animal from which the cells were prepared.


2015 ◽  
Vol 56 (1) ◽  
pp. 216-227 ◽  
Author(s):  
Youhua Wang ◽  
Shiran Zhou ◽  
Hua Xu ◽  
Shixian Yan ◽  
Dawei Xu ◽  
...  

2003 ◽  
Vol 19 (2) ◽  
pp. 119-123 ◽  
Author(s):  
S. Geuna ◽  
S. Raimondo ◽  
S. Nicolino ◽  
E. Boux ◽  
M. Fornaro ◽  
...  

1989 ◽  
Vol 108 (2) ◽  
pp. 607-611 ◽  
Author(s):  
P W Mason ◽  
J W Bigbee ◽  
G H DeVries

Proliferation of Schwann cells is one of the first events that occurs after contact with a growing axon. To further define the distribution and properties of this axonal mitogen, we have (a) cocultured cerebellar granule cells, which lack glial ensheathment in vivo with Schwann cells; and (b) exposed Schwann cell cultures to isolated granule cell membranes. Schwann cells cocultured with granule cells had a 30-fold increase in the labeling index over Schwann cells cultured alone, suggesting that the mitogen is located on the granule cell surface. Inhibition of granule cell proteoglycan synthesis caused a decrease in the granule cells' ability to stimulate Schwann cell proliferation. Membranes isolated from cerebellar granule cells when added to Schwann cell cultures caused a 45-fold stimulation in [3H]thymidine incorporation. The granule cell mitogenic signal was heat and trypsin sensitive and did not require lysosomal processing by Schwann cells to elicit its proliferative effect. The ability of granule cells and their isolated membranes to stimulate Schwann cell proliferation suggests that the mitogenic signal for Schwann cells is a ubiquitous factor present on all axons regardless of their ultimate state of glial ensheathment.


1995 ◽  
Vol 129 (3) ◽  
pp. 789-796 ◽  
Author(s):  
L Cheng ◽  
M Khan ◽  
A W Mudge

Schwann cells in culture divide in response to defined mitogens such as PDGF and glial growth factor (GGF), but proliferation is greatly enhanced if agents such as forskolin, which increases Schwann cell intracellular cAMP, are added at the same time as PDGF or GGF (Davis, J. B., and P. Stroobant. 1990. J. Cell Biol. 110:1353-1360). The effect of forskolin is probably due to an increase in numbers of PDGF receptors (Weinmaster, G., and G. Lemke. 1990. EMBO (Eur. Mol. Biol. Organ.) J. 9:915-920. Neuropeptides and beta-adrenergic agonists have been reported to have no effect on potentiating the mitogenic response of either PDGF or GGF. We show that the neuropeptide calcitonin gene-related peptide (CGRP) increases Schwann cell cAMP levels, but the cells rapidly desensitize. We therefore stimulated the cells in pulsatile fashion to partly overcome the effects of desensitization and show that CGRP can synergize with PDGF to stimulate Schwann cell proliferation, and that CGRP is as effective as forskolin in the pulsatile regime. CGRP is a good substrate for the neutral endopeptidase 24.11. Schwann cells in vivo have this protease on their surface, so the action of CGRP could be terminated by this enzyme and desensitization prevented. We therefore suggest that CGRP may play an important role in stimulating Schwann cell proliferation by regulating the response of mitogenic factors such as PDGF.


Neuroreport ◽  
2007 ◽  
Vol 18 (7) ◽  
pp. 669-673 ◽  
Author(s):  
Per Gustavsson ◽  
Cecilia Eriksson Linsmeier ◽  
Hakon Leffler ◽  
Martin Kanje

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