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Wnt/β‐catenin signaling can influence the proliferation and differentiation of progenitor populations in the hippocampus and subventricular zone, known germinal centers in the adult mouse brain. It is not known whether β‐catenin signaling occurs in quiescent glial progenitors in cortex or spinal cord, nor is it known whether β‐catenin is involved in the activation of glial progenitor populations after injury. Using a β‐catenin reporter mouse (BATGAL mouse), we show that β‐catenin signaling occurs in NG2 chondroitin sulfate proteoglycan+ (NG2) progenitors in the cortex, in subcallosal zone (SCZ) progenitors, and in subependymal cells surrounding the central canal. Interestingly, cells with β‐catenin signaling increased in the cortex and SCZ following traumatic brain injury (TBI) but did not following spinal cord injury. Initially after TBI, β‐catenin signaling was predominantly increased in a subset of NG2+ progenitors in the cortex. One week following injury, the majority of β‐catenin signaling appeared in reactive astrocytes but not oligodendrocytes. Bromodeoxyuridine (BrdU) paradigms and Ki‐67 staining showed that the increase in β‐catenin signaling occurred in newly born cells and was sustained after cell division. Dividing cells with β‐catenin signaling were initially NG2+; however, by four days after a single injection of BrdU, they were predominantly astrocytes. Infusing animals with the mitotic inhibitor cytosine arabinoside prevented the increase of β‐catenin signaling in the cortex, confirming that the majority of β‐catenin signaling after TBI occurs in newly born cells. These data argue for manipulating the Wnt/β‐catenin pathway after TBI as a way to modify post‐traumatic gliogenesis. S TEM  C ELLS  2010;28:297–307

β‐Catenin Signaling Increases in Proliferating NG2+ Progenitors and Astrocytes during Post‐Traumatic Gliogenesis in the Adult Brain