Fig. 1

Schematic overview of distinct molecular programs regulating neural stem cell plasticity in adult zebrafish pallium during homeostasis, traumatic injury, and neurodegeneration. In homeostatic constitutive neurogenesis Fezf2 [50], Notch3 [49], miR-9 [53], and Estrogen [54] favor quiescence of neural stem cells where Notch1 [49] promotes proliferation Upon traumatic injuries, acute inflammation induces the plasticity of neural stem cells through LTC4 [42], Gata3 [41], and Cxcr5 [40] signaling, and Id1 [44] restores quiescence of neural stem cells. After Amyloid-mediated neurodegeneration, IL4 through phospho-STAT6 signaling is required for neural stem cell proliferation [37]. Please note that the programs required for neural stem cell plasticity in homeostatic conditions may also be employed after injuries or neurodegeneration; however, the programs in non-physiological conditions of injury and disease are specific to those damage paradigms and are not required for plasticity in homeostatic conditions. Redevelopmental programs are turned on for new neurons to differentiate and develop into respective cell types. For extensive reviews, please see [2, 13, 16, 19, 20, 29, 30, 39, 45, 46, 55]