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 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 S100ß and fibroblast growth factor-2 are present in cultured Schwann cells and may exert paracrine actions on the peripheral nerve injury

2008 ◽  
Vol 23 (6) ◽  
pp. 555-560 ◽  
Author(s):  
Tatiana Duobles ◽  
Thais de Sousa Lima ◽  
Beatriz de Freitas Azevedo Levy ◽  
Gerson Chadi
Keyword(s):  
Growth Factor ◽  
Sciatic Nerve ◽  
Fibroblast Growth Factor ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Satellite Cells ◽  
Peripheral Nerves ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Cultured Schwann Cells

PURPOSE: The neurotrophic factor fibroblast growth factor-2 (FGF-2, bFGF) and Ca++ binding protein S100ß are expressed by the Schwann cells of the peripheral nerves and by the satellite cells of the dorsal root ganglia (DRG). Recent studies have pointed out the importance of the molecules in the paracrine mechanisms related to neuronal maintenance and plasticity of lesioned motor and sensory peripheral neurons. Moreover, cultured Schwann cells have been employed experimentally in the treatment of central nervous system lesions, in special the spinal cord injury, a procedure that triggers an enhanced sensorymotor function. Those cells have been proposed to repair long gap nerve injury. METHODS: Here we used double labeling immunohistochemistry and Western blot to better characterize in vitro and in vivo the presence of the proteins in the Schwann cells and in the satellite cells of the DRG as well as their regulation in those cells after a crush of the rat sciatic nerve. RESULTS: FGF-2 and S100ß are present in the Schwann cells of the sciatic nerve and in the satellite cells of the DRG. S100ß positive satellite cells showed increased size of the axotomized DRG and possessed elevated amount of FGF-2 immunoreactivity. Reactive satellite cells with increased FGF-2 labeling formed a ring-like structure surrounding DRG neuronal cell bodies.Reactive S100ß positive Schwann cells of proximal stump of axotomized sciatic nerve also expressed higher amounts of FGF-2. CONCLUSION: Reactive peripheral glial cells synthesizing FGF-2 and S100ß may be important in wound repair and restorative events in the lesioned peripheral nerves.

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.

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

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 Schwann cell autophagy, myelinophagy, initiates myelin clearance from injured nerves

2015 ◽  
Vol 210 (1) ◽  
pp. 153-168 ◽  
Author(s):  
Jose A. Gomez-Sanchez ◽  
Lucy Carty ◽  
Marta Iruarrizaga-Lejarreta ◽  
Marta Palomo-Irigoyen ◽  
Marta Varela-Rey ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Peripheral Nerves ◽  
Wallerian Degeneration ◽  
Molecular Mechanisms ◽  
Demyelinating Disease ◽  
Cell Reprogramming ◽  
Selective Autophagy ◽  
Wide Range

Although Schwann cell myelin breakdown is the universal outcome of a remarkably wide range of conditions that cause disease or injury to peripheral nerves, the cellular and molecular mechanisms that make Schwann cell–mediated myelin digestion possible have not been established. We report that Schwann cells degrade myelin after injury by a novel form of selective autophagy, myelinophagy. Autophagy was up-regulated by myelinating Schwann cells after nerve injury, myelin debris was present in autophagosomes, and pharmacological and genetic inhibition of autophagy impaired myelin clearance. Myelinophagy was positively regulated by the Schwann cell JNK/c-Jun pathway, a central regulator of the Schwann cell reprogramming induced by nerve injury. We also present evidence that myelinophagy is defective in the injured central nervous system. These results reveal an important role for inductive autophagy during Wallerian degeneration, and point to potential mechanistic targets for accelerating myelin clearance and improving demyelinating disease.

Local production of serum amyloid a is implicated in the induction of macrophage chemoattractants in Schwann cells during wallerian degeneration of peripheral nerves

Glia ◽  
2012 ◽  
Vol 60 (10) ◽  
pp. 1619-1628 ◽  
Author(s):  
So Young Jang ◽  
Yoon Kyung Shin ◽  
Ha Young Lee ◽  
Joo Youn Park ◽  
Duk Joon Suh ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Peripheral Nerves ◽  
Wallerian Degeneration ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Local Production ◽  
Amyloid A

The Recovery of Peripheral Nerves following Tissue Expansion

1992 ◽  
Vol 17 (1) ◽  
pp. 78-85 ◽  
Author(s):  
R. H. MILNER ◽  
P. R. WILKINS
Keyword(s):  
Sciatic Nerve ◽  
Histological Examination ◽  
Conduction Velocity ◽  
Peripheral Nerves ◽  
Axonal Degeneration ◽  
Recovery Period ◽  
Tissue Expansion ◽  
Segmental Demyelination ◽  
Nerve Model ◽  
The Mean

A rat sciatic nerve model has been used to study the response of nerves to tissue expansion and their recovery at intervals up to 100 days using electrophysiology and histological methods. Tissue expansion has been shown to increase nerve length by 32% of which half remained at 100 days. Following tissue expansion the mean conduction velocity of the sciatic nerve was reduced to 30.0 ± 1.35 m/s which represented 60.3% of control values, by 100 days the conduction velocity had almost returned to normal. Histological examination showed the cause of the reduction in function to be due to segmental demyelination without axonal degeneration, these changes returned towards normal during the recovery period but were not completely reversed by 100 days.

scholarly journals Ndrg1-Deficient Mice Exhibit a Progressive Demyelinating Disorder of Peripheral Nerves

2004 ◽  
Vol 24 (9) ◽  
pp. 3949-3956 ◽  
Author(s):  
Tomohiko Okuda ◽  
Yujiro Higashi ◽  
Koichi Kokame ◽  
Chihiro Tanaka ◽  
Hisato Kondoh ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Schwann Cells ◽  
Peripheral Nerves ◽  
Sensory Neuropathy ◽  
Disease Type ◽  
Charcot Marie Tooth ◽  
Charcot Marie Tooth Disease ◽  
Hind Limbs ◽  
Deficient Mice ◽  
Tooth Disease

ABSTRACT NDRG1 is an intracellular protein that is induced under a number of stress and pathological conditions, and it is thought to be associated with cell growth and differentiation. Recently, human NDRG1 was identified as a gene responsible for hereditary motor and sensory neuropathy-Lom (classified as Charcot-Marie-Tooth disease type 4D), which is characterized by early-onset peripheral neuropathy, leading to severe disability in adulthood. In this study, we generated mice lacking Ndrg1 to analyze its function and elucidate the pathogenesis of Charcot-Marie-Tooth disease type 4D. Histological analysis showed that the sciatic nerve of Ndrg1-deficient mice degenerated with demyelination at about 5 weeks of age. However, myelination of Schwann cells in the sciatic nerve was normal for 2 weeks after birth. Ndrg1-deficient mice showed muscle weakness, especially in the hind limbs, but complicated motor skills were retained. In wild-type mice, NDRG1 was abundantly expressed in the cytoplasm of Schwann cells rather than the myelin sheath. These results indicate that NDRG1 deficiency leads to Schwann cell dysfunction, suggesting that NDRG1 is essential for maintenance of the myelin sheaths in peripheral nerves. These mice will be used for future analyses of the mechanisms of myelin maintenance.

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