scholarly journals Cyclic Stretch of Either PNS or CNS Located Nerves Can Stimulate Neurite Outgrowth

Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 32
Author(s):  
Vasileios Kampanis ◽  
Bahardokht Tolou-Dabbaghian ◽  
Luming Zhou ◽  
Wolfgang Roth ◽  
Radhika Puttagunta

The central nervous system (CNS) does not recover from traumatic axonal injury, but the peripheral nervous system (PNS) does. We hypothesize that this fundamental difference in regenerative capacity may be based upon the absence of stimulatory mechanical forces in the CNS due to the protective rigidity of the vertebral column and skull. We developed a bioreactor to apply low-strain cyclic axonal stretch to adult rat dorsal root ganglia (DRG) connected to either the peripheral or central nerves in an explant model for inducing axonal growth. In response, larger diameter DRG neurons, mechanoreceptors and proprioceptors showed enhanced neurite outgrowth as well as increased Activating Transcription Factor 3 (ATF3).

2020 ◽  
Vol 40 (8) ◽  
pp. 1327-1338
Author(s):  
Nicholas Hanuscheck ◽  
Andrea Schnatz ◽  
Carine Thalman ◽  
Steffen Lerch ◽  
Yvonne Gärtner ◽  
...  

Abstract Neurons of the central nervous system (CNS) that project long axons into the spinal cord have a poor axon regenerative capacity compared to neurons of the peripheral nervous system. The corticospinal tract (CST) is particularly notorious for its poor regeneration. Because of this, traumatic spinal cord injury (SCI) is a devastating condition that remains as yet uncured. Based on our recent observations that direct neuronal interleukin-4 (IL-4) signaling leads to repair of axonal swellings and beneficial effects in neuroinflammation, we hypothesized that IL-4 acts directly on the CST. Here, we developed a tissue culture model for CST regeneration and found that IL-4 promoted new growth cone formation after axon transection. Most importantly, IL-4 directly increased the regenerative capacity of both murine and human CST axons, which corroborates its regenerative effects in CNS damage. Overall, these findings serve as proof-of-concept that our CST regeneration model is suitable for fast screening of new treatments for SCI.


2003 ◽  
Vol 26 (3) ◽  
pp. 209-224 ◽  
Author(s):  
Rafael Luján ◽  
Carlos de Cabo de la Vega ◽  
Eduardo Dominguez del Toro ◽  
Juan J Ballesta ◽  
Manuel Criado ◽  
...  

2009 ◽  
Vol 65 ◽  
pp. S41
Author(s):  
Kazunori Sango ◽  
Hiroko Yanagisawa ◽  
Shizuka Takaku ◽  
Yukari Komuta ◽  
Hitoshi Kawano ◽  
...  

2018 ◽  
Vol 19 (1) ◽  
pp. 50-64 ◽  
Author(s):  
Yiting Yin ◽  
Xin Qi ◽  
Yuan Qiao ◽  
Huaxiang Liu ◽  
Zihan Yan ◽  
...  

Background: The notion that proteasome inhibitor bortezomib (BTZ) induced intracellular oxidative stress resulting in peripheral neuropathy has been generally accepted. The association of mitochondrial dysfunction, cell apoptosis, and endoplasmic reticulum (ER) stress with intracellular oxidative stress is ambiguous and still needs to be investigated. The activation of activating transcription factor 3 (ATF3) is a stress-hub gene which was upregulated in dorsal root ganglion (DRG) neurons after different kinds of peripheral nerve injuries. Objective: To investigate a mechanism underlying the action of BTZ-induced intracellular oxidative stress, mitochondrial dysfunction, cell apoptosis, and ER stress via activation of ATF3. </P><P> Methods: Primary cultured DRG neurons with BTZ induced neurotoxicity and DRG from BTZ induced painful peripheral neuropathic rats were used to approach these questions. Results: BTZ administration caused the upregulation of ATF3 paralleled with intracellular oxidative stress, mitochondrial dysfunction, cell apoptosis, and ER stress in DRG neurons both in vitro and in vivo. Blocking ATF3 signaling by small interfering RNA (siRNA) gene silencing technology resulted in decreased intracellular oxidative stress, mitochondrial dysfunction, cell apoptosis, and ER stress in DRG neurons after BTZ treatment. This study exhibited important mechanistic insight into how BTZ induces neurotoxicity through the activation of ATF3 resulting in intracellular oxidative stress, mitochondrial dysfunction, cell apoptosis, and ER stress and provided a novel potential therapeutic target by blocking ATF3 signaling.


Development ◽  
1962 ◽  
Vol 10 (2) ◽  
pp. 115-126
Author(s):  
R. T. Sims

The literature on regeneration in the central nervous system of vertebrates has been reviewed exhaustively by Windle (1955, 1956). Adult fish and urodeles reestablish physiological and anatomical continuity of the spinal cord after it has been completely transected while adult anurans (Piatt & Piatt, 1958) and mammals on the whole do not. In all groups of vertebrates regeneration is more successful in the period of early embryonic development, and becomes less so as development proceeds. Experiments designed to investigate the factors responsible for this change demand an animal in which the difference in the regenerative capacity of embryonic and adult form is marked, and all stages of development are easily accessible for operative procedures. These criteria are satisfied by Anura. For this reason regeneration in the anuran central nervous system merits further investigation. After spinal cord transection in urodele larvae, Piatt (1955) found that the Mauthner axons did not regenerate although other axons around them did.


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