Morphological changes in spinal motor neurons giving rise to long-term regenerated sciatic nerve axons

1988 ◽  
Vol 463 (1) ◽  
pp. 69-77 ◽  
Author(s):  
C.M. Bowe ◽  
C.H. Yu ◽  
S.G. Waxman
2004 ◽  
Vol 153 (2) ◽  
pp. 251-260 ◽  
Author(s):  
Harutoshi Sakakima ◽  
Yoshihiro Yoshida ◽  
Kenji Kadomatsu ◽  
Yukio Yuzawa ◽  
Seiichi Matsuo ◽  
...  

2007 ◽  
Vol 421 (2) ◽  
pp. 152-157 ◽  
Author(s):  
Haruno Suzuki ◽  
Koujiro Tohyama ◽  
Kizashi Nagata ◽  
Shigeru Taketani ◽  
Masasuke Araki

2007 ◽  
Vol 26 (8) ◽  
pp. 2151-2159 ◽  
Author(s):  
A.E. King ◽  
T.C. Dickson ◽  
C.A. Blizzard ◽  
S.S. Foster ◽  
R.S. Chung ◽  
...  

2001 ◽  
Vol 93 (2) ◽  
pp. 199-208 ◽  
Author(s):  
Alexander K Murashov ◽  
Ihtsham Ul Haq ◽  
Charles Hill ◽  
Eunice Park ◽  
Michael Smith ◽  
...  

2019 ◽  
Author(s):  
Kazuhide Asakawa ◽  
Hiroshi Handa ◽  
Koichi Kawakami

AbstractCytoplasmic aggregation of TDP-43 characterizes degenerating neurons in most cases of amyotrophic lateral sclerosis (ALS), yet the mechanisms and cellular outcomes of TDP-43 pathology remain largely elusive. Here, we develop an optogenetic TDP-43 variant (opTDP-43), whose multimerization status can be modulated in vivo through external light illumination. Using the translucent zebrafish neuromuscular system, we demonstrate that short-term light stimulation reversibly induces cytoplasmic opTDP-43 mislocalization, but not aggregation, in the spinal motor neuron, leading to an axon outgrowth defect associated with myofiber denervation. In contrast, opTDP-43 forms pathological aggregates in the cytoplasm after longer-term illumination and seeds non-optogenetic TDP-43 aggregation. Furthermore, we find that an ALS-linked mutation in the intrinsically disordered region (IDR) exacerbates the light-dependent opTDP-43 toxicity on locomotor behavior. Together, our results propose that IDR-mediated TDP-43 oligomerization triggers both acute and long-term pathologies of motor neurons, which may be relevant to the pathogenesis and progression of ALS.


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