Autophagic myelin destruction by schwann cells during wallerian degeneration and segmental demyelination

Glia ◽  
2015 ◽  
Vol 64 (5) ◽  
pp. 730-742 ◽  
Author(s):  
So Young Jang ◽  
Yoon Kyung Shin ◽  
So Young Park ◽  
Joo Youn Park ◽  
Hye Jeong Lee ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Wallerian Degeneration ◽  
Segmental Demyelination

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.

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.

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.

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

scholarly journals Interleukin-6 is required for the early induction of glial fibrillary acidic protein in Schwann cells during Wallerian degeneration

2009 ◽  
Vol 108 (3) ◽  
pp. 776-786 ◽  
Author(s):  
Hyun Kyoung Lee ◽  
In Ae Seo ◽  
Duk Joon Suh ◽  
Jeong-In Hong ◽  
Young Hyun Yoo ◽  
...  
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Schwann Cells ◽  
Interleukin 6 ◽  
Wallerian Degeneration ◽  
Acidic Protein

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.

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