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    • Overall our data support the view that the SEZ is

    2018-10-26

    Overall, our data support the view that the SEZ is a source of plasticity for the adult CC, and that oligodendroblasts could be a valid therapeutic tool for demyelinating diseases if their generation from wider parts of the SEZ could be stimulated, if their response could be sustained for long periods, and if the reasons that lead to variable levels of remyelination capacity between different models of demyelination are elucidated. They also complement recently reported evidence that different pools of OPCs contribute in discrete and specific ways to remyelination (Crawford et al., 2016). Finally, they highlight the fact that pOPCs manifest an advantage in generating oligodendrocytes when compared with SEZ oligodendrogenesis and that this does not change in the aging brain.
    Experimental Procedures
    Author Contributions
    Acknowledgments The authors thank Prof. Frank Kirchhoff (University of Saarland, Germany) for the kind supply of the transgenic mice and Dr. Francisco Rivera (Paracelcus University, Salzburg) for the kind supply of sections from nestin-CreErt2 x Rosa26-EYFP mice. This work was supported by a grant from the Biotechnology and Biological Sciences Research Council (UK) (BB/I013210/1) to R.F. and I.K.
    Introduction Different types of rna polymerase ii injuries, such as ischemia or trauma, have been reported to influence adult neurogenesis in the two stem cell niches of the adult brain (Arvidsson et al., 2002; Takasawa et al., 2002). In the subventricular zone (SVZ), these injuries lead to enhanced proliferation and migration of neuroblasts, not only to the olfactory bulb but also toward the damaged area. Interestingly, brain tumors, such as glioblastoma, also stimulate the migration of immature precursor cells toward the tumor mass, as these cells can be found at the tumor edge (Chirasani et al., 2010; Glass et al., 2005). A neurogenic response to pathologies such as stroke (Jin et al., 2006; Macas et al., 2006), Huntington disease (Curtis et al., 2003), epilepsy (Crespel et al., 2005), or brain tumors (Macas et al., 2014) has also been reported in adult human brains. These results have fueled hope of using the activation of endogenous neural stem cells in response to injury as an additional strategy for the treatment of neurological diseases (Lindvall and Kokaia, 2006). Recent findings of ongoing neurogenesis in the adult human striatum and hippocampus (Ernst et al., 2014; Spalding et al., 2013) have lent further support to this prospect. Multiple factors and signaling pathways have been described as playing a role in the injury reaction of the SVZ. Among the most prominent are the Notch signaling pathway and the SDF-1α ligand and its receptor CXCR4 (Imitola et al., 2004). Notch is reported to upregulate the proliferation and differentiation of cells in the SVZ in a stroke model, while SDF-1α has been shown to influence the direction of migration toward injured regions. However, the question of which signals, emanating from the injury site, are responsible for initiating the injury reaction of neural stem cells (NSCs) in the SVZ has received little attention. Such a signal would require the fulfillment of several criteria: Firstly, it has to be transmitted quickly, as changes in gene expression in the murine SVZ occur as early as 4 hr after the lesion (Wang et al., 2009b). Secondly, the signal must be relayed over relatively large distances, arguing against diffusible factors. Thirdly, the signal must be spatially orientated, as changes in the SVZ largely occur in the hemisphere, ipsilateral but not contralateral to the injury. Finally, it must be self-sustainable. By analyzing gene expression patterns in the SVZ 48 hr after permanent middle cerebral artery occlusion (MCAO) in mice, we found a prominent change in the expression levels of calcium-binding proteins based on gene ontology (GO) classification, indicating a possible role of calcium signaling in the initiation of the injury reaction. Together with other observations, this led us to the hypothesis that information about an injury induced by stroke may be transmitted to the SVZ by traveling astrocytic calcium waves, transient increases in intracellular calcium that transmit to adjacent non-stimulated astrocytes and thereby spread over long distances (Scemes and Giaume, 2006). Calcium waves display a wide range of physiological functions in the brain. In development, calcium increases have been shown to modulate cell division, neuronal differentiation, and migration (Owens and Kriegstein, 1998; Stroh et al., 2011). More recently, it has been shown that postnatal neural stem and progenitor cells (NSPCs) in the SVZ can communicate with astrocytes via gap junction-mediated calcium waves (Lacar et al., 2011), and calcium signaling in the adult SVZ has been shown to modulate blood vessel dilation (Lacar et al., 2012). However, to the best of our knowledge, a mechanism by which distant signals from injuries can be relayed by astrocytic networks to NSCs has not been described.