scholarly journals Ubiquitin Expression in Degenerating Axons of Equine Cervical Compressive Myelopathy

1996 ◽  
Vol 33 (3) ◽  
pp. 356-359 ◽  
Author(s):  
B. S. Jortner ◽  
W. K. Scarratt ◽  
P. D. Modransky ◽  
A. Walton ◽  
S. K. Perkins
Keyword(s):  
Wallerian Degeneration ◽  
Stress Protein ◽  
Nerve Fibers ◽  
Axonal Swelling ◽  
Myelinated Nerve ◽  
Cervical Compressive Myelopathy ◽  
Compressive Myelopathy ◽  
Young Horses ◽  
Catabolic Process ◽  
Degenerating Axons

Neuropathologic examination revealed axonal swelling and breakdown leading to Wallerian degeneration of affected myelinated nerve fibers in the spinal cord white matter of four young horses with equine cervical compressive myelopathy. Immunohistochemical reactions for the cell stress protein ubiquitin revealed an enhanced presence in the swollen axons, which may reflect a role for ubiquitin in the neuronal catabolic process of axonal compression and degeneration in this myelopathy.

scholarly journals GSK3B-mediated phosphorylation of MCL1 regulates axonal autophagy to promote Wallerian degeneration

2017 ◽  
Vol 216 (2) ◽  
pp. 477-493 ◽  
Author(s):  
Shuji Wakatsuki ◽  
Shinji Tokunaga ◽  
Megumi Shibata ◽  
Toshiyuki Araki
Keyword(s):  
Wallerian Degeneration ◽  
Axonal Degeneration ◽  
Physiological Function ◽  
Glycogen Synthase ◽  
Bcl2 Family ◽  
Adenosine Triphosphate Production ◽  
Bcl2 Family Member ◽  
Catabolic Process ◽  
Degenerating Axons

Macroautophagy is a catabolic process, in which portions of cytoplasm or organelles are delivered to lysosomes for degradation. Emerging evidence has indicated a pathological connection between axonal degeneration and autophagy. However, the physiological function and induction mechanism of autophagy in axons remain elusive. We herein show that, through activation of BECLIN1, glycogen synthase kinase 3B (GSK3B)–mediated phosphorylation of BCL2 family member MCL1 induces axonal autophagy and axonal degeneration. Phosphorylated MCL1 is ubiquitinated by the FBXW7 ubiquitin ligase and degraded by the proteasome, thereby releasing BECLIN1 to induce axonal autophagy. Axonal autophagy contributes to local adenosine triphosphate production in degenerating axons and the exposure of phosphatidylserine—an “eat-me” signal for phagocytes—on transected axons and is required for normal recruitment of phagocytes to axonal debris in vivo. These results suggest that GSK3B–MCL1 signaling to regulate autophagy might be important for the successful completion of Wallerian degeneration.

HISTOMETRIC AND ULTRASTRUCTURAL ORGANIZATION OF THE NERVIMUSCULAR TERMINALS OF SKELETAL MUSCLES AT A HYPOKINESIA

2019 ◽  
pp. 55-63
Author(s):  
Z. M. Yaschyshyn ◽  
S. L. Popel
Keyword(s):  
Skeletal Muscles ◽  
Structural Adjustment ◽  
Muscle Fibers ◽  
Electron Microscopic Examination ◽  
Nerve Fibers ◽  
Ultrastructural Changes ◽  
Ultrastructural Organization ◽  
Electron Microscopic ◽  
Myelinated Nerve ◽  
Male Wistar Rats

The aim: to study the dynamics of histological and ultrastructural changes in muscle fibers and their neuromuscular endings under conditions of prolonged hypokinesia at different stages of ontogenesis. Methods. Studied skeletal muscles and their peripheral nervous apparatus of laboratory male Wistar rats aged 30 to 270 days. The restriction of motor activity was carried out in special canister cells for 30, 60, 90, and 240 days (5 animals for each term). To determine the type of muscle fiber, the Nahlas histochemical method was used, the Kulchitsky method was used to detect myelinated nerve fibers, the Bilshovsky-Gros method and the electron microscopic method to identify neuromuscular endings. Results. The data of histological and electron microscopic examination of skeletal muscle fibers and their neuromuscular endings under conditions of prolonged hypokinesia indicate their regular restructuring during the development of muscles, the formation of their synapses and structures that are associated with them at different stages of ontogenesis. Conclusion. The study provides an in-depth understanding of the relative frequency and nature of the disturbance of the neuromuscular endings during prolonged hypokinesia and its effect on the dynamics of structural adjustment of individual types of muscle fibers in ontogenesis.

HISTOMETRIC AND ULTRASTRUCTURAL ORGANIZATION OF THE NERVIMUSCULAR TERMINALS OF SKELETAL MUSCLES AT A HYPOKINESIA

2019 ◽  
pp. 55-63
Author(s):  
Z. M. Yaschyshyn ◽  
S. L. Popel
Keyword(s):  
Skeletal Muscles ◽  
Structural Adjustment ◽  
Muscle Fibers ◽  
Electron Microscopic Examination ◽  
Nerve Fibers ◽  
Ultrastructural Changes ◽  
Ultrastructural Organization ◽  
Electron Microscopic ◽  
Myelinated Nerve ◽  
Male Wistar Rats

The aim: to study the dynamics of histological and ultrastructural changes in muscle fibers and their neuromuscular endings under conditions of prolonged hypokinesia at different stages of ontogenesis. Methods. Studied skeletal muscles and their peripheral nervous apparatus of laboratory male Wistar rats aged 30 to 270 days. The restriction of motor activity was carried out in special canister cells for 30, 60, 90, and 240 days (5 animals for each term). To determine the type of muscle fiber, the Nahlas histochemical method was used, the Kulchitsky method was used to detect myelinated nerve fibers, the Bilshovsky-Gros method and the electron microscopic method to identify neuromuscular endings. Results. The data of histological and electron microscopic examination of skeletal muscle fibers and their neuromuscular endings under conditions of prolonged hypokinesia indicate their regular restructuring during the development of muscles, the formation of their synapses and structures that are associated with them at different stages of ontogenesis. Conclusion. The study provides an in-depth understanding of the relative frequency and nature of the disturbance of the neuromuscular endings during prolonged hypokinesia and its effect on the dynamics of structural adjustment of individual types of muscle fibers in ontogenesis.

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