Optimal conditions for graft survival and reinnervation of denervated muscles after embryonic motoneuron transplantation into peripheral nerves undergoing Wallerian degeneration

2021 ◽  
Author(s):  
Hideyoshi Sawada ◽  
Shigeru Kurimoto ◽  
Katsuhiro Tokutake ◽  
Sota Saeki ◽  
Hitoshi Hirata
Keyword(s):  
Graft Survival ◽  
Peripheral Nerves ◽  
Wallerian Degeneration ◽  
Optimal Conditions ◽  
Denervated Muscles

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 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.

Desert hedgehog-patched 2 expression in peripheral nerves during Wallerian degeneration and regeneration

2006 ◽  
Vol 66 (3) ◽  
pp. 243-255 ◽  
Author(s):  
Sepideh N. Bajestan ◽  
Fujio Umehara ◽  
Yuko Shirahama ◽  
Kayoko Itoh ◽  
Soheila Sharghi-Namini ◽  
...  
Keyword(s):  
Peripheral Nerves ◽  
Wallerian Degeneration ◽  
Desert Hedgehog

Proliferation of mast cells in peripheral nerves during wallerian degeneration

1969 ◽  
Vol 13 (2) ◽  
pp. 111-121 ◽  
Author(s):  
Yngve Olsson ◽  
Johan Sj�strand
Keyword(s):  
Mast Cells ◽  
Peripheral Nerves ◽  
Wallerian Degeneration

Early events of peripheral nerve regeneration

2005 ◽  
Vol 2 (2) ◽  
pp. 139-147 ◽  
Author(s):  
DAVID MCDONALD ◽  
CHU CHENG ◽  
YUANYUAN CHEN ◽  
DOUGLAS ZOCHODNE
Keyword(s):  
Peripheral Nerve ◽  
Peripheral Nerves ◽  
Wallerian Degeneration ◽  
De Novo ◽  
Peripheral Nerve Regeneration ◽  
Confocal Imaging ◽  
Double Labeling ◽  
Proximal Stump ◽  
Cell Processes ◽  
Early Regeneration

Early regeneration of injured peripheral nerves involves a series of events that are important in the success of eventual reconnection. In many nerve injuries, such as transections with gaps, axons and Schwann cells (SCs) penetrate into new microenvironments de novo, not involving zones of Wallerian degeneration. We studied unexplored axon–SC interactions by sampling of newly forming connections through a silicone conduit across transected rat sciatic peripheral nerve gaps. Axon and SC participation in bridge formation was addressed by light microscopy, electron microscopy and by double-labeling immunohistochemistry, including confocal imaging, and several, less appreciated aspects of early regrowth were identified. There are limitations to early and widespread regeneration of axons and SCs into bridges initially formed from connective tissue and blood vessels. Regrowth is ‘staggered’ such that only a small percentage of parent axons sampled the early bridge. There is an intimate, almost invariable relationship between SCs and extension of axons, which challenges the concept that axons lead and SCs follow. ‘Naked’ axons were infrequent and limited in scope. Axons did not seek out and adhere to vascular laminin but intimately followed laminin deposits associated with apposed SCs. Growth cones identified by labeling of β III tubulin, PGP 9.5 and GAP43/B50 were complex, implying a pause in their regrowth, and were most prominent at the proximal stump–regenerative bridge interface. There is surprising and substantial hostility to local regrowth of axons into newly forming peripheral nerve bridges. Early axon outgrowth, associated with apposed Schwann cell processes, is highly constrained even when not exposed to adjacent myelin and products of Wallerian degeneration.

Neural determination of muscle fibre numbers in embryonic rat lumbrical muscles

Development ◽  
1987 ◽  
Vol 100 (3) ◽  
pp. 395-409 ◽  
Author(s):  
J.J. Ross ◽  
M.J. Duxson ◽  
A.J. Harris
Keyword(s):  
Peripheral Nerves ◽  
Nerve Terminals ◽  
Normal Numbers ◽  
Myotube Formation ◽  
Physical Presence ◽  
Lumbrical Muscle ◽  
Lumbrical Muscles ◽  
Denervated Muscles ◽  
Intrinsic Muscles

The generation and development of muscle cells in the IVth hindlimb lumbrical muscle of the rat was studied following total or partial denervation. Denervation was carried out by injection of beta-bungarotoxin (beta-BTX), a neurotoxin which binds to and destroys peripheral nerves. Primary myotubes were generated in denervated muscles and reached their normal stable number on embryonic day 17 (E17). This number was not maintained and denervated muscles examined on E19 or E21 contained many degenerating primary myotubes. Embryos injected with beta-bungarotoxin (beta-BTX) on E12 or E13 suffered a partial loss of motoneurones, resulting in a reduced number of axons in the L4 ventral root (the IVth lumbrical muscle is supplied by axons in L4, L5 and L6 ventral roots) and reduced numbers of nerve terminals in the intrinsic muscles of the hindfoot. Twitch tension measurements showed that all myotubes in partly innervated muscles examined on E21 contracted in response to nerve stimulation. Primary myotubes were formed and maintained at normal numbers in muscles with innervation reduced throughout development, but a diminished number of secondary myotubes formed by E21. The latter was correlated with a reduction in number of mononucleate cells within the muscles. If beta-BTX was injected on E18 to denervate muscles after primary myotube formation was complete, E21 embryo muscles contained degenerating primary myotubes. After injection to denervate muscles on E19, the day secondary myotubes begin to form, E21 muscles possessed normal numbers of primary myotubes. In both cases, secondary myotube formation had stopped about 1 day after the injection and the number of mononucleate cells was greatly reduced, indicating that cessation of secondary myotube generation was most probably due to exhaustion of the supply of competent myoblasts. We conclude that nerve terminals regulate the number of secondary myotubes by stimulating mitosis in a nerve-dependent population of myoblasts and that activation of these myoblasts requires the physical presence of nerve terminals as well as activation of contraction in primary myotubes.

Biomaterials for Repairing Gaps After Peripheral Nerve Injury

2021 ◽  
Vol 13 (4) ◽  
pp. 530-536
Author(s):  
Dong-Xu Huang ◽  
Jiang-Nan Li ◽  
Ge-Yi Zhang ◽  
Wen-Gang Wang ◽  
Lei Xia ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerves ◽  
Peripheral Nerve Injury ◽  
Wallerian Degeneration ◽  
Standard Treatment ◽  
Spontaneous Recovery ◽  
Nerve Conduits ◽  
Advanced Biomaterials ◽  
Review Current

Peripheral nerves have complex and precise structures that differ from other types of tissues and intrinsic regeneration abilities after injury. Spontaneous recovery is possible for neuropraxia and axonotmesis, while surgical treatment is required for neurotmesis. It remains a challenge to repair nerve gaps, a series of severe neurotmesis. It seems that 3 cm is the upper limit distance for primate peripheral nerves to regenerate spontaneously. Nerve autografts are the gold standard treatment for bridging nerve gaps. In the present review, current biomaterials for repairing gaps after peripheral nerve injury are briefly summarized. Moreover, the microstructure of the peripheral nerve, classifications of peripheral nerve injury, and the Wallerian degeneration are reviewed in the biological view and clinical practice. The failure of nerve regeneration in nerve conduits bridging longer than 3 cm gaps may be contributing to the insufficient vascularization of nerve conduit materials. Future researchers could focus on advanced biomaterials that promoting the angiogenesis of nerve conduits.

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.

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