In mammals, many diseases of the central nervous system (CNS) are associated with substantial neuronal loss. However, the adult brain has a very limited capacity for compensatory neurogenesis. In the cerebral cortex, progenitor like cells could be identified at sites of injury, but the default differentiation of these cells is the glial phenotype. A key issue is therefore to identify regulators that could be manipulated to promote neurogenesis and replacement of lost neurons. The canonical Wnt signaling is required for embryonic neurogenesis in the cerebral cortex. However, the role of this signaling in generating newborn neurons at postnatal ages remains poorly understood. As a first step to address this question, we investigated the effects of canonical/β-catenin signaling on cultured neural progenitors (NPCs) isolated from the rat subventricular zone (SVZ) at P0-1. We used lentiviral overexpression of canonical Wnt elements and studied the effects of gain or loss of function …