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Abstract
Neural stem cells (NSCs) are crucial for development, regeneration, and repair of the nervous system. Most NSCs in mammalian adult brains are quiescent, but in response to extrinsic stimuli, they can exit from quiescence and become reactivated to give rise to new neurons. The delicate balance between NSC quiescence and activation is important for adult neurogenesis and NSC maintenance. However, how NSCs transit between quiescence and activation remains largely elusive. Here, we discuss our current understanding of the molecular mechanisms underlying the reactivation of quiescent NSCs. We review recent advances on signaling pathways originated from the NSC niche and their crosstalk in regulating NSC reactivation. We also highlight new intrinsic paradigms that control NSC reactivation in Drosophila and mammalian systems. We also discuss emerging evidence on modeling human neurodevelopmental disorders using NSCs.
Highlights
The ability of stem cells to switch between quiescence and proliferation is crucial for tissue homeostasis and regeneration
In the mammalian adult brain, radial glial cells are neural stem cells (NSCs) that reside within the ventricular–subventricular zone (V–SVZ)/subependymal zone (SEZ) in the walls of the lateral ventricles, while radial glial cells are NSCs located in the subgranular zone (SGZ) of the hippocampal dentate gyrus (Fig 1) [5, 6]
While extrinsic niche-derived cues allow NSCs to reactivate in respond to changes in the external environment such as the presence of nutrition, exercise, drug administration, or injury, intrinsic mechanisms represent another facet of control that is dependent on nuclear factors and cellcycle regulators within NSCs during their reactivation
Summary
Most NSCs in mammalian adult brains are quiescent, but in response to extrinsic stimuli, they can exit from quiescence and become reactivated to give rise to new neurons. The delicate balance between NSC quiescence and activation is important for adult neurogenesis and NSC maintenance. How NSCs transit between quiescence and activation remains largely elusive. We discuss our current understanding of the molecular mechanisms underlying the reactivation of quiescent NSCs. We review recent advances on signaling pathways originated from the NSC niche and their crosstalk in regulating NSC reactivation. We highlight new intrinsic paradigms that control NSC reactivation in Drosophila and mammalian systems. We discuss emerging evidence on modeling human neurodevelopmental disorders using NSCs
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