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.

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 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 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.

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

1970 ◽  
Vol 7 (5) ◽  
pp. 420-434 ◽  
Author(s):  
K. M. Charlton ◽  
K. R. Pierce
Keyword(s):  
Electron Microscopy ◽  
Sciatic Nerve ◽  
Schwann Cells ◽  
Active Transport ◽  
Peripheral Nerves ◽  
Wallerian Degeneration ◽  
Light And Electron Microscopy ◽  
Segmental Demyelination ◽  
Femoral Site ◽  
Oral Doses

Lesions in peripheral nerves from 12 goats poisoned experimentally with coyotillo were studied by light and electron microscopy. The goats were poisoned with daily oral doses of the ground coyotillo fruits and killed at various times after the first day of dosing. Lesions at a mid-femoral site of the sciatic nerve included swelling of Schwann cells, degeneration of mitochondria, depletion of glycogen, splitting of myelin, segmental demyelination, and Wallerian degeneration. The results were suggestive of primary mitochondrial injury in Schwann cells with resultant impaired active transport, intracellular edema, splitting of myelin, and segmental demyelination.

scholarly journals Major cellular events in peripheral nerve regeneration: A brief overview

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Naidu M ◽  
David P
Keyword(s):  
Peripheral Nerve ◽  
Schwann Cells ◽  
Wallerian Degeneration ◽  
Peripheral Nerve Regeneration ◽  
Scar Tissue ◽  
Regenerative Process ◽  
Cellular Events ◽  
Neural Cell Adhesion ◽  
Proximal Stump ◽  
Regeneration Response

Injury to a peripheral nerve leads to degeneration of the segment distal to the site of lesion, a process referred to as Wallerian degeneration. During Wallerian degeneration, axons and myelin sheaths undergo degeneration and are phagocytosed by macrophages and Schwann cells. The Schwann cells proliferate and the endoneurial tubes persist, together the whole structure is known as the band of Büngner. Within few hours, the damaged axons in the proximal stump initiate a regeneration response, with formation of new growth cones. During Wallerian degeneration, neurotrophins, neural cell adhesion molecules, cytokines and other soluble factors are upregulated to facilitate regeneration. The recovery of the target in mammals is often variable, but almost never complete. In humans, scar tissue forms at the site of lesion and this often results in poor recovery of the target. The major events underlying this regenerative process is highlighted and discussed in this review.

scholarly journals ATP Release through Lysosomal Exocytosis from Peripheral Nerves: The Effect of Lysosomal Exocytosis on Peripheral Nerve Degeneration and Regeneration after Nerve Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Junyang Jung ◽  
Hyun Woo Jo ◽  
Hyunseob Kwon ◽  
Na Young Jeong
Keyword(s):  
Peripheral Nerve ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Peripheral Nerves ◽  
Wallerian Degeneration ◽  
Atp Release ◽  
Nerve Degeneration ◽  
Peripheral Neurons ◽  
Charcot Marie Tooth Disease ◽  
Axonal Degradation

Studies have shown that lysosomal activation increases in Schwann cells after nerve injury. Lysosomal activation is thought to promote the engulfment of myelin debris or fragments of injured axons in Schwann cells during Wallerian degeneration. However, a recent interpretation of lysosomal activation proposes a different view of the phenomenon. During Wallerian degeneration, lysosomes become secretory vesicles and are activated for lysosomal exocytosis. The lysosomal exocytosis triggers adenosine 5′-triphosphate (ATP) release from peripheral neurons and Schwann cells during Wallerian degeneration. Exocytosis is involved in demyelination and axonal degradation, which facilitate nerve regeneration following nerve degeneration. At this time, released ATP may affect the communication between cells in peripheral nerves. In this review, our description of the relationship between lysosomal exocytosis and Wallerian degeneration has implications for the understanding of peripheral nerve degenerative diseases and peripheral neuropathies, such as Charcot-Marie-Tooth disease or Guillain-Barré syndrome.

Adhesion and proliferation are enhanced in vitro in Schwann cells from nerve undergoing wallerian degeneration

1991 ◽  
Vol 29 (3) ◽  
pp. 308-318 ◽  
Author(s):  
A. Komiyama ◽  
D. L. Novicki ◽  
Kinuko Suzuki
Keyword(s):  
Schwann Cells ◽  
Wallerian Degeneration

Role of ornithine decarboxylase in proliferation of schwann cells during wallerian degeneration and its enhancement by nerve expansion

1995 ◽  
Vol 18 (11) ◽  
pp. 1341-1343 ◽  
Author(s):  
H. Hirata ◽  
H. Hibasami ◽  
T. Hineno ◽  
D. Shi ◽  
A. Morita ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Ornithine Decarboxylase ◽  
Wallerian Degeneration
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