Abstract
External stimuli such as injury, learning, or stress influence the production of neurons by neural stem cells (NSCs) in the adult mammalian brain. These external stimuli directly impact stem cell activity by influencing areas directly connected or in close proximity to the neurogenic niches of the adult brain. However, very little is known on how distant injuries affect NSC activation state. In this study, we demonstrate that a thoracic spinal transection injury activates the distally located hippocampal-NSCs. This activation leads to a transient increase production of neurons that functionally integrate to improve animal’s performance in hippocampal-related memory tasks. We further show that interferon-CD95 signaling is required to promote injury-mediated activation of remote NSCs. Thus, we identify an immune-CNS axis responsible for injury-mediated activation of remotely located NSCs.
Highlights
The process of generating new neurons in the adult mouse brain is best characterized in the ventricular-subventricular zone (V-SVZ) and the subgranular zone (SGZ) of the dentate gyrus (DG)
In order to detect the reaction of SGZ-neural stem cells (NSCs) and their neurogenic progeny, we labeled these cells with BrdU at the time of injury and in the following 24 h, 48 h or after 89 days and examined them at 2 days, 2 weeks, 4 weeks and 13 weeks following injury (Figure 1A)
Brains were stained for BrdU, to follow actively dividing NSCs and transient amplifying progenitors (TAPs) cells on their transition to BrdU+/DCX+ neuroblasts and BrdU+/NeuN+ newborn neurons (Figure 1B)
Summary
The process of generating new neurons in the adult mouse brain is best characterized in the ventricular-subventricular zone (V-SVZ) and the subgranular zone (SGZ) of the dentate gyrus (DG). Neural stem cells (NSCs) within the V-SVZ generate neuronal precursors that migrate along the rostral migratory stream into the olfactory bulbs (OBs) where they disperse radially and generate functional interneurons that fine-tune odor discrimination. NSCs within the SGZ generate neuronal precursors that migrate short distance into the inner granule cell layer of the DG where they become functionally integrated into the existing network (Gage, 2000; Taupin and Gage, 2002; Zhao et al, 2008; Ming and Song, 2011; Aimone et al, 2014; Lim and Alvarez-Buylla, 2016). Endogenous NSCs can be activated by traumatic brain injury (Arvidsson et al, 2002; Parent et al, 2002; Thored et al, 2006; Hou et al, 2008; Liu et al, 2009)
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