scholarly journals Multimodal imaging of subventricular zone neural stem/progenitor cells in the cuprizone mouse model reveals increased neurogenic potential for the olfactory bulb pathway, but no contribution to remyelination of the corpus callosum

NeuroImage ◽  
2014 ◽  
Vol 86 ◽  
pp. 99-110 ◽  
Author(s):  
Caroline Guglielmetti ◽  
Jelle Praet ◽  
Janaki Raman Rangarajan ◽  
Ruth Vreys ◽  
Nathalie De Vocht ◽  
...  
2020 ◽  
Vol 15 (10) ◽  
pp. 1773 ◽  
Author(s):  
Giuseppe Lupo ◽  
Giancarlo Poiana ◽  
Roberta Gioia ◽  
Serena Sineri ◽  
Silvia Cardarelli ◽  
...  

2015 ◽  
Vol 93 (8) ◽  
pp. 1203-1214 ◽  
Author(s):  
Chiara Soldati ◽  
Pasquale Caramanica ◽  
Matthew J. Burney ◽  
Camilla Toselli ◽  
Angela Bithell ◽  
...  

2018 ◽  
Vol 40 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Masae Naruse ◽  
Koji Shibasaki ◽  
Hiroya Shimauchi-Ohtaki ◽  
Yasuki Ishizaki

Neuroblasts derived from neural stem cells (NSCs) in the subventricular zone (SVZ) migrate along the rostral migratory stream into the olfactory bulb to generate interneurons under normal physiological conditions. When demyelination occurs, NSCs or neural progenitor cells (NPCs) in the SVZ provide newly formed oligodendrocytes to demyelinated lesions. The plasticity of NSC/NPC lineages may tend to oligodendrogenesis under the influence of demyelinated lesions. The mechanisms, however, still remain unknown. This study revealed that focal demyelination in the corpus callosum caused activation of the microglia, not only at the site of demyelination but also in the SVZ, and dramatically increased the generation of oligodendrocyte progenitor cells (OPCs) in the SVZ. Furthermore, the inhibition of microglial activation by minocycline treatment decreased OPC generation in the SVZ, suggesting that microglial activation in the SVZ, induced by the focal demyelination in the corpus callosum, regulates NSC/NPC lineage plasticity in situ. In contrast to the findings regarding demyelination in the corpus callosum, inducing focal demyelination in the internal capsule did not induce either microglial activation or OPC generation in the SVZ. These results suggest that the mechanism of OPC generation in the SVZ after inducing demyelinating lesions could be different across the demyelinated regions.


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