Proliferation and Glia-Directed Differentiation of Neural Stem Cells in the Subventricular Zone of the Lateral Ventricle and the Migratory Pathway to the Lesions after Cortical Devascularization of Adult Rats

Abstract

We investigated the effects of cortical devascularization on the proliferation, differentiation, and migration of neural stem cells (NSCs) in the subventricular zone (SVZ) of the lateral ventricle of adult rats. 60 adult male Wistar rats were randomly divided into control group and devascularized group. At 15 and 30 days after cerebral cortices were devascularized, rats were euthanized and immunohistochemical analysis was performed. The number of PCNA-, Vimentin-, and GFAP-positive cells in the bilateral SVZ of the lateral wall and the superior wall of the lateral ventricles of 15- and 30-day devascularized groups increased significantly compared with the control group (P < 0.05 and P < 0.01). The area density of PCNA-, Vimentin-, and GFAP-positive cells in cortical lesions of 15- and 30-day devascularized groups increased significantly compared with the control group (P < 0.05 and P < 0.01). PCNA-, GFAP-, and Vimentin-positive cells in the SVZ migrated through the rostral migratory stream (RMS), and PCNA-, GFAP-, and Vimentin-positive cells from both the ipsilateral and contralateral dorsolateral SVZ (dl-SVZ) migrated into the corpus callosum (CC) and accumulated, forming a migratory pathway within the CC to the lesioned site. Our study suggested that cortical devascularization induced proliferation, glia-directed differentiation, and migration of NSCs from the SVZ through the RMS or directly to the corpus callosum and finally migrating radially to cortical lesions. This may play a significant role in neural repair.

New Neurons in the Post-ischemic and Injured Brain: Migrating or Resident?

“…Neuroblasts stretch out their leading processes in the direction of the zone to which they are moving (Parent et al, 2002; Zhang et al, 2004; Dayer et al, 2005; Osman et al, 2011; Nakaguchi et al, 2012; Moraga et al, 2014). Moreover, migrating neuroblasts often integrate into chains, and the orientation of the chain also corresponds to the direction of migration (Parent et al, 2002; Zhang et al, 2004; Wang et al, 2007; Kuge et al, 2009; Yan et al, 2009b; Kazanis et al, 2013; Wan et al, 2016; Song et al, 2017). Alternatively, clustering cells with round cell bodies, lacking long leading processes and co-expressing DCX with proliferation marker Ki67 are considered as non-migrating local NPCs (Magnusson et al, 2014; Nato et al, 2015).…”

“…distribution pattern of neuroblasts migrating from the SVZ/PPV to the damaged area in fixed brain slices (Magavi et al, 2000; Parent et al, 2002; Jin et al, 2003; Chen et al, 2004; Goings et al, 2004; Gotts and Chesselet, 2005; Ramaswamy et al, 2005; Zhang et al, 2005; Ohab et al, 2006; Kolb et al, 2007; Leker et al, 2007; Wang et al, 2007; Yan et al, 2007; Faiz et al, 2008, 2015; Li et al, 2008, Li B. et al, 2010; Li et al, 2011; Kreuzberg et al, 2010; Osman et al, 2011; Saha et al, 2013; Yi et al, 2013; Moraga et al, 2014; Vandeputte et al, 2014; Wan et al, 2016; Palma-Tortosa et al, 2017; Pradillo et al, 2017; Song et al, 2017; Tseng et al, 2018);…”

“…In this section we consider several works that describe interhemispheric migration of neuroblasts after cortical injury (Ramaswamy et al, 2005; Wan et al, 2016). The authors discovered that damage to the cortex may result in migration of neuroblasts from one hemisphere to the other.…”

“…The authors discovered that damage to the cortex may result in migration of neuroblasts from one hemisphere to the other. While Wan et al (2016) reported on migration from the healthy hemisphere to the damaged one, Ramaswamy et al (2005) discussed migration from damaged to healthy.…”

“…Wan et al (2016) observed that after cortical devascularization, migration occurs not only from the SVZ of the same hemisphere, but also from the contralateral SVZ, to the injured cortex. In fixed brain slices, the authors observed distribution of cells migrating from the contralateral SVZ via the midline, further to the ipsilateral corpus callosum, and finally to the lesion area in the cortex.…”