The Ror-family of receptor tyrosine kinases (RTKs), Ror1 and Ror2, have been shown to play crucial roles in the developmental morphogenesis by acting as receptors or co-receptors to mediate Wnt5a-induced signaling. Although Ror1, Ror2, and Wnt5a are expressed in the developing brain, little is known about their roles in the neural development. Here we show that Ror1, Ror2, and their ligand Wnt5a are highly expressed in neocortical neural progenitor cells (NPCs). siRNA-mediated suppression of Ror1, Ror2, or Wnt5a in cultured NPCs isolated from embryonic neocortex results in the reduction of βIII-tubulin-positive neurons that are produced from NPCs possibly through the generation of T-box brain 2 (Tbr2)-positive intermediate progenitors. BrdU-labeling experiments further reveal that proportion of proliferative and neurogenic NPCs, that are positive for neural progenitor cell marker (Pax6), but negative for glial cell marker (glial fibrillary acidic protein; GFAP), is reduced within a few days in culture following knockdown of these molecules, suggesting that Ror1, Ror2, and Wnt5a regulate neurogenesis through the maintenance of NPCs. Moreover, we show that Dishevelled2 (Dvl2) is involved in Wnt5a–Ror1 and Wnt5a–Ror2 signalings in NPCs, and that suppressed expression of Dvl2 indeed reduces the proportion of proliferative and neurogenic NPCs. Interestingly, suppressed or forced expression of either Ror1 or Ror2 in NPCs in the developing neocortex results in their precocious or delayed differentiation into neurons, respectively. Collectively, these results indicate that Wnt5a–Ror1 and Wnt5a–Ror2 signalings play roles in maintaining proliferative and neurogenic NPCs during neurogenesis of the developing neocortex.