scholarly journals Myelin sheath survival after guanethidine-induced axonal degeneration.

1992 ◽  
Vol 116 (2) ◽  
pp. 395-403 ◽  
Author(s):  
G J Kidd ◽  
J W Heath ◽  
B D Trapp ◽  
P R Dunkley
Keyword(s):  
Schwann Cells ◽  
Superior Cervical Ganglion ◽  
Myelin Sheath ◽  
Axonal Regeneration ◽  
Wallerian Degeneration ◽  
Axonal Degeneration ◽  
Serial Sections ◽  
Myelin Sheaths ◽  
Cervical Ganglion ◽  
Contrast Analysis

Membrane-membrane interactions between axons and Schwann cells are required for initial myelin formation in the peripheral nervous system. However, recent studies of double myelination in sympathetic nerve have indicated that myelin sheaths continue to exist after complete loss of axonal contact (Kidd, G. J., and J. W. Heath. 1988. J. Neurocytol. 17:245-261). This suggests that myelin maintenance may be regulated either by diffusible axonal factors or by nonaxonal mechanisms. To test these hypotheses, axons involved in double myelination in the rat superior cervical ganglion were destroyed by chronic guanethidine treatment. Guanethidine-induced sympathectomy resulted in a Wallerian-like pattern of myelin degeneration within 10 d. In doubly myelinated configurations the axon, inner myelin sheath (which lies in contact with the axon), and approximately 75% of outer myelin sheaths broke down by this time. Degenerating outer sheaths were not found at later periods. It is probably that outer sheaths that degenerated were only partially displaced from the axon at the commencement of guanethidine treatment. In contrast, analysis of serial sections showed that completely displaced outer internodes remained ultrastructurally intact. These internodes survived degeneration of the axon and inner sheath, and during the later time points (2-6 wk) they enclosed only connective tissue elements and reorganized Schwann cells/processes. Axonal regeneration was not observed within surviving outer internodes. We therefore conclude that myelin maintenance in the superior cervical ganglion is not dependent on direct axonal contact or diffusible axonal factors. In addition, physical association of Schwann cells with the degenerating axon may be an important factor in precipitating myelin breakdown during Wallerian degeneration.

Schwann Cell Reactions in Acute and Chronic Segmental Demyelinating Neuropathies

1968 ◽  
Vol 26 ◽  
pp. 108-109
Author(s):  
Roy O. Weller
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Schwann Cells ◽  
Myelin Sheath ◽  
Wallerian Degeneration ◽  
Demyelinating Disease ◽  
Segmental Demyelination ◽  
Recovery Stage ◽  
Myelin Sheaths ◽  
Demyelinating Neuropathies

The length of axon that each Schwann cell myelinates in a normal peripheral nerve is approximately proportional to the diameter of the axon and the thickness of the myelin sheath produced. When segmental demyelination occurs, individual segments, represented by the length of axon covered by one Schwann cell, lose their myelin sheaths but the axons are preserved. This differs from Wallerian degeneration where myelin destruction occurs along the length of a nerve fibre following death of the axon.In experimental diphtheritic neuropathy, an acute segmental demyelinating disease, lysosomes accumulate within the Schwann cells prior to disruption of the myelin sheath; furthermore, the site of initial myelin breakdown appears to be closely related to the collections of lysosomes. The Schwann cell starts to form a new myelin sheath around the axon probably within a few hours of the destruction of the original myelin sheath, and while the latter is being catabolised within lysosomal vacuoles This stage of remyelination follows a similar course to primary myelination, so that the recovery stage is characterised by normal axons with either no myelin, or surrounded by sheaths that are very thin relative to the diameter of the axon.

scholarly journals A Neuropathy in Goats Caused by Experimental Coyotillo (Karwinskia humboldtiana) Poisoning

1970 ◽  
Vol 7 (5) ◽  
pp. 385-407 ◽  
Author(s):  
K. M. Charlton ◽  
K. R. Pierce
Keyword(s):  
Schwann Cells ◽  
Myelin Sheath ◽  
Wallerian Degeneration ◽  
Axonal Degeneration ◽  
Cell Injury ◽  
Transitional Zone ◽  
Primary Lesion ◽  
Segmental Demyelination ◽  
Sequential Development ◽  
Oral Doses

The sequential development of the lesions in the peripheral nervous systems of 22 goats poisoned with daily oral doses of ground coyotillo fruits was studied. Studies of teased fibers revealed swelling of Schwann cells, clefts in the myelin sheath, segmental demyelination, remyelination, Wallerian degeneration, and regeneration. A few fibers had a large globular or ovoid swelling in a transitional zone between a region undergoing segmental demyelination at one end and Wallerian degeneration at the other end. These distended transitional zones were the sites of intense acid phosphatase activity in axons. These histologic studies indicate that the primary lesion occurred in Schwann cells and resulted in swelling of Schwann cells, clefts in the myelin sheath, and segmental demyclination. The sequence of development of the lesions suggests that axonal degeneration were secondary to Schwann-cell injury.

Periaxin expression in myelinating Schwann cells: modulation by axon-glial interactions and polarized localization during development

Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4265-4273 ◽  
Author(s):  
S.S. Scherer ◽  
Y.T. Xu ◽  
P.G. Bannerman ◽  
D.L. Sherman ◽  
P.J. Brophy
Keyword(s):  
Cell Membrane ◽  
Membrane Protein ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Protein Interactions ◽  
Myelin Sheath ◽  
Myelin Proteins ◽  
Developmentally Regulated ◽  
Protein Levels ◽  
Myelin Sheaths

Periaxin is a newly described protein that is expressed exclusively by myelinating Schwann cells. In developing nerves, periaxin is first detected as Schwann cells ensheathe axons, prior to the appearance of the proteins that characterize the myelin sheath. Periaxin is initially concentrated in the adaxonal membrane (apposing the axon) but, during development, as myelin sheaths mature, periaxin becomes predominately localized at the abaxonal Schwann cell membrane (apposing the basal lamina). In permanently axotomized adult nerves, periaxin is lost from the abaxonal and adaxonal membranes, becomes associated with degenerating myelin sheaths and is phagocytosed by macrophages. In crushed nerves, in which axons regenerate and are remyelinated, periaxin is first detected in the adoxonal membrane as Schwann cells ensheathe regenerating axons, but again prior to the appearance of other myelin proteins. Periaxin mRNA and protein levels change in parallel with those of other myelin-related genes after permanent axotomy and crush. These data demonstrate that periaxin is expressed by myelinating Schwann cells in a dynamic, developmentally regulated manner. The shift in localization of periaxin in the Schwann cell after completion of the spiralization phase of myelination suggests that periaxin participates in membrane-protein interactions that are required to stabilize the mature myelin sheath.

scholarly journals A BIOCHEMICAL AND MORPHOLOGIC STUDY OF MYELINATION AND DEMYELINATION

1958 ◽  
Vol 108 (2) ◽  
pp. 197-214 ◽  
Author(s):  
Guido Majno ◽  
Manfred L. Karnovsky
Keyword(s):  
Schwann Cells ◽  
Myelin Sheath ◽  
Wallerian Degeneration ◽  
Distal Portion ◽  
Histological Findings ◽  
Cellular Reaction ◽  
Morphologic Study ◽  
Normal Rat ◽  
Regenerating Nerve

Bilateral transection was performed on rat sciatics. At varying intervals after the operation, samples of nerve were taken both distal and proximal to the level of transection, as well as from the tissue which bridged the gap between the stumps. These samples were incubated in Warburg flasks, with glucose and a labelled lipide precursor (acetate or phosphate). The total lipides were then extracted and their radioactivity was measured. Normal rat sciatics served as controls, and the biochemical and histological findings were correlated. In the distal portion undergoing Wallerian degeneration, the lipide content began to fall before any removal of myelin could be detected histologically. It is suggested that there is a period of "non-cellular removal" prior to the physical breakdown of the myelin. Changes in respiration and in lipogenesis from acetate followed a triphasic course, and agreed with the histological findings in that after a period of predominantly passive changes (approximately 1 to 3 days) there follows a period of cellular reaction (4 to 50 days) and a period of atrophy (from 50 days onward). The incorporation of phosphate into the lipides was increased at all stages examined, even as early as 22 hours after section. This increased P32 incorporation could not be reproduced in nerves allowed to degenerate in vitro. It is suggested that the hypertrophying Schwann cells synthesize some lipide moieties at a considerably faster rate than others. Proximal to the level of transection, lipogenesis from acetate was depressed, for as long as 32 days postoperatively. It appears, therefore, that the maintenance of the myelin sheath is impaired also above the level of transection. In the "union tissue" which developed between the stumps, prior to the appearance of histologically visible myelin, lipogenesis was low; later it rose above levels for normal nerve. This pattern of lipogenesis in regenerating nerve is similar to that found in growing nerves.

scholarly journals ELECTRON MICROSCOPIC OBSERVATIONS ON ALLERGIC ENCEPHALOMYELITIS IN THE RABBIT

1960 ◽  
Vol 112 (5) ◽  
pp. 735-742 ◽  
Author(s):  
Sarah A. Luse ◽  
David B. McDougal
Keyword(s):  
Electron Microscopy ◽  
White Matter ◽  
Myelin Sheath ◽  
Wallerian Degeneration ◽  
Bovine Brain ◽  
Allergic Encephalomyelitis ◽  
Electron Microscopic ◽  
Inflammatory Infiltration ◽  
Myelin Sheaths ◽  
Spinal Roots

Allergic encephalomyelitis was produced in rabbits by injection of white matter from bovine brain plus adjuvants. Electron microscopy revealed focal demyelinization in both the spinal roots and cord. The peripheral lesions were characterized by vacuolization of Schwann cytoplasm, destruction of the myelin sheath, and by some appearances suggesting remyelinization. In the cord there was a marked perivascular inflammatory infiltration with focal destruction of the blood-brain barrier as demonstrated by formation of an abnormal interstitial space about capillaries. Mitochondria of oligodendroglia were strikingly swollen whereas those of other cells were morphologically normal. Axons were denuded of their myelin sheaths and the myelin detritus sequestered within gitter cells. Fibrous astrocytic gliosis occurred to some degree. Focal evidences of myelin reformation were noted centrally as well as peripherally. Allergic encephalomyelitis, as a primary demyelinating lesion, is contrasted with Wallerian degeneration in which myelin degeneration is secondary to destruction of the axon.

The components of regrowing nerves which support the regeneration of irradiated salamander limbs

Development ◽  
1972 ◽  
Vol 28 (2) ◽  
pp. 419-435
Author(s):  
H. Wallace
Keyword(s):  
Brachial Plexus ◽  
Schwann Cells ◽  
Myelin Sheath ◽  
Wallerian Degeneration ◽  
Series Of Experiments

Forelimbs of juvenile axolotls do not regenerate when amputated in a previously irradiated region. They usually do regenerate, however, if they have also been denervated shortly after irradiation and well before amputation. Five series of experiments are reported which define the conditions permitting this paradoxical regeneration. Crushing the nerves of the brachial plexus proved a satisfactory means of causing temporary denervation. Shielding any region of the arm or shoulder, during an irradiation that preceded such denervation, permits regeneration to occur at a region which was initially irradiated. Lengths of brachial nerve implanted into an irradiated arm also support its regeneration. It is concluded that temporary denervation (including Wallerian degeneration and the regrowth of axons) mobilizes cells in a shielded region of the arm. These cells migrate both proximally and distally, so that some come to occupy the site of amputation. Schwann cells of the myelin sheath are identified as the cells most likely to behave in this way. It thus seems probable that those non-irradiated Schwann cells which occupy a generally irradiated limbstump can form the exclusive source of a mesenchymal blastema and the various internal tissues of the regenerate.

Evidence for a Blood Ganglion Barrier in the Superior Cervical Ganglion of the Rat

1982 ◽  
Vol 40 ◽  
pp. 204-204
Author(s):  
D. M. DePace
Keyword(s):  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Peripheral Nerves ◽  
Time Schedule ◽  
Transmission Electron ◽  
Cervical Ganglion ◽  
The Central Nervous System ◽  
Cervical Ganglia ◽  
Capillary Circulation ◽  
And Control

The majority of blood vessels in the superior cervical ganglion possess a continuous endothelium with tight junctions. These same features have been associated with the blood brain barrier of the central nervous system and peripheral nerves. These vessels may perform a barrier function between the capillary circulation and the superior cervical ganglion. The permeability of the blood vessels in the superior cervical ganglion of the rat was tested by intravenous injection of horseradish peroxidase (HRP). Three experimental groups of four animals each were given intravenous HRP (Sigma Type II) in a dosage of.08 to.15 mg/gm body weight in.5 ml of.85% saline. The animals were sacrificed at five, ten or 15 minutes following administration of the tracer. Superior cervical ganglia were quickly removed and fixed by immersion in 2.5% glutaraldehyde in Sorenson's.1M phosphate buffer, pH 7.4. Three control animals received,5ml of saline without HRP. These were sacrificed on the same time schedule. Tissues from experimental and control animals were reacted for peroxidase activity and then processed for routine transmission electron microscopy.

scholarly journals Biology of the repair of central nervous system demyelinated lesions: an appraisal

1996 ◽  
Vol 54 (2) ◽  
pp. 331-334 ◽  
Author(s):  
L. A. V Peireira ◽  
M. A. Cruz-Höfling ◽  
M. S. J. Dertkigil ◽  
D. L. Graça
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cells ◽  
Demyelinating Disease ◽  
Experimental Models ◽  
Primitive Cell ◽  
Marked Influence ◽  
Myelin Sheaths ◽  
Human Material ◽  
The Central Nervous System

The integrity of myelin sheaths is maintained by oligodendrocytes and Schwann cells respectively in the central nervous system (CNS) and in the peripheral nervous system. The process of demyelination consisting of the withdrawal of myelin sheaths from their axons is a characteristic feature of multiple sclerosis, the most common human demyelinating disease. Many experimental models have been designed to study the biology of demyelination and remyelination (repair of the lost myelin) in the CNS, due to the difficulties in studying human material. In the ethidium bromide (an intercalating gliotoxic drug) model of demyelination, CNS remyelination may be carried out by surviving oligodendrocytes and/or by cells differentiated from the primitive cell lines or either by Schwann cells that invade the CNS. However, some factors such as the age of the experimental animals, intensity and time of exposure to the intercalating chemical and the topography of the lesions have marked influence on the repair of the tissue.

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