Retarded Wallerian degeneration following peripheral nerve transection in C57BL/6/Ola mice is associated with delayed down-regulation of the P0 gene

1991 ◽  
Vol 538 (1) ◽  
pp. 157-160 ◽  
Author(s):  
C.E. Thomson ◽  
L.S. Mitchell ◽  
I.R. Griffiths ◽  
S. Morrison
Keyword(s):  
Peripheral Nerve ◽  
Wallerian Degeneration ◽  
Nerve Transection ◽  
Down Regulation

scholarly journals Effects of Taxol on Regeneration in a Rat Sciatic Nerve Transection Model

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Shih-Tien Hsu ◽  
Chun-Hsu Yao ◽  
Yuan-Man Hsu ◽  
Jia-Horng Lin ◽  
Yung-Hsiang Chen ◽  
...  
Keyword(s):  
Growth Factors ◽  
Sciatic Nerve ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Nerve Transection ◽  
Cremophor El ◽  
Neuronal Connectivity ◽  
Sciatic Nerve Transection ◽  
Expression Levels ◽  
Nerve Growth Factors

Abstract Recent studies describe taxol as a candidate treatment for promoting central nerve regeneration. However, taxol has serious side effects including peripheral neurotoxicity, and little information is known about the effect of taxol on peripheral nerve regeneration. We investigated the effects of taxol on regeneration in a rat sciatic nerve transection model. Rats were divided into four groups (n = 10): normal saline (i.p.) as the control, Cremophor EL vehicle, and 2 or 6 mg/kg of taxol in the Cremophor EL solution (four times in day-2, 4, 6, and 8), respectively. We evaluated neuronal electrophysiology, animal behaviour, neuronal connectivity, macrophage infiltration, location and expression levels of calcitonin gene-related peptide (CGRP), and expression levels of both nerve growth factors and immunoregulatory factors. In the high-dose taxol group (6 mg/kg), neuronal electrophysiological function was significantly impaired. Licking latencies were significantly changed while motor coordination was unaffected. Neuronal connectivity, macrophage density, and expression levels of CGRP was dramatically reduced. Expression levels of nerve growth factors and immunoregulatory factors was also reduced, while it was increased in the low-dose taxol group (2 mg/kg). These results indicate that taxol can modulate local inflammatory conditions, impair nerve regeneration, and impede recovery of a severe peripheral nerve 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 Early changes in muscle atrophy and muscle fiber type conversion after spinal cord transection and peripheral nerve transection in rats

2013 ◽  
Vol 10 (1) ◽  
pp. 46 ◽  
Author(s):  
Kosaku Higashino ◽  
Tetsuya Matsuura ◽  
Katsuyoshi Suganuma ◽  
Kiminori Yukata ◽  
Toshihiko Nishisho ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Peripheral Nerve ◽  
Muscle Atrophy ◽  
Muscle Fiber ◽  
Fiber Type ◽  
Spinal Cord Transection ◽  
Muscle Fiber Type ◽  
Nerve Transection ◽  
Type Conversion

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.

Sortilins in neuropathic pain

2012 ◽  
Vol 3 (3) ◽  
pp. 183-184
Author(s):  
M. Richner ◽  
O.J. Bjerrum ◽  
Y. De Koninck ◽  
A. Nykjaer ◽  
C.B. Vaegter
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Mechanical Allodynia ◽  
Molecular Mechanisms ◽  
Intrathecal Injection ◽  
Ion Concentration ◽  
Down Regulation

AbstractBackground/aimsThe molecular mechanisms underlying neuropathic pain are incompletely understood, but recent data suggest that down-regulation of the chloride extruding co-transporter KCC2 in spinal cord sensory neurons is critical: Following peripheral nerve injury, activated microglia in the spinal cord release BDNF, which stimulates neuronal TrkB receptors and ultimately results in the reduction of KCC2 levels. Consequently, neuronal intracellular chloride ion concentration increases, impairing GABAA-receptor mediated inhibition. We have previously described how the receptor sortilin modulates neurotrophin signaling by facilitating anterograde transport of Trk receptors. Unpublished data further link SorCS2, another member of the Sortilins family of sorting receptors (sortilin, SorLA and SorCS1–3) to BDNF signaling by regulating presynaptic TrkB trafficking. The purpose of this study is to explore the involvement of Sortilins in neuropathic pain.MethodsWe subjected wild-type (wt), sortilin knockout (Sort1-/-) and SorCS2 knockout (SorCS2-/-) mice to the Spared Nerve Injury (SNI) model of peripheral nerve injury. Mechanical allodynia was measured by von Frey filaments using the up-down-up method and a 3-out-of-5 thresshold.ResultsAs previously described by several groups, wt mice developed significant mechanical allodynia following SNI. Interestingly however, mice lacking sortilin or SorCS2 were fully protected from development of allodynia and did not display KCC2 down-regulation following injury. In addition, a single intrathecal injection of antibodies against sortilin or SorCS2 could delay or rescue mechanical allodynia in wt SNI mice for 2-3 days. Finally, neither sortilin nor SorCS2 deficient mice responded to intrathecal injection of BDNF, in contrast to wt mice which developed transient mechanical allodynia.ConclusionWe hypothesize that sortilin and SorCS2 are involved in neuropathic pain development by regulating TrkB signaling. Alternatively, Sortilins may directly influence the regulation of KCC2 membrane levels following injury. Both hypotheses are currently being investigated by our group.

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