Thus, if the environment in the ischemic striatum does not change, the new neurons cannot survive. Wnt family gene mRNA is detected in the SVZ, but there is no upregulation of these genes after stroke. Nevertheless, endogenous Wnt signaling is probably important for cell proliferation in the SVZ during Rapamycin mTOR inhibitor stroke, considering the decreased proliferation caused by beta-catenin siRNA after middle cerebral artery occlusion. Thus, although Wnt signaling is an important pathway in the SVZ after stroke, it does not naturally upregulate in the reactive SVZ in order to compensate the neuronal damage. Yet, as shown by this study, we can still activate and use the Wnt signaling pathway in our model. The present study was a proof of concept study to evaluate Wnt3a treatment using the endothelin-1 focal ischemia model. The advantages of this model over the middle cerebral artery occlusion are its simplicity and inherent reliability. A further study using the MCAo model is needed to understand the clinical relevance of these results. In conclusion, the results of our study show that lentivirusmediated gene and neurogenesis in the striatum after focal ischemic injury. These findings have important therapeutic implications and should prompt further studies on the use of Wnt signaling to improve functional outcome in patients with stroke. Rab GTPases regulate intracellular membrane trafficking in all eukaryotic cells. Several Rab GTPases have become standard markers for specific subcellular membrane compartments, yet the function of the majority of rab GTPases is still unknown. Mutations in rab genes and their regulators cause several hereditary and neurological diseases including Griscelli syndrome, Charcot-Marie-Tooth type 2B disease, Warburg Micro Syndrome, X-linked mental retardation and Hermansky-Pudlak syndrome. Rab8-dependent trafficking underlies Bardet-Biedl syndrome, which causes retinopathy and blindness. In Drosophila, post-Golgi trafficking of rhodopsin and guidance receptors during brain wiring depends on Rab11. Lastly, active zone assembly at synapses requires Rab3, the best known neuronal Rab GTPase. The human genome contains at least 60 and maybe more than 70 rab genes. The Drosophila genome contains 33 potential rab GTPase loci based on primary sequence homology, 23 of which have direct orthologs in humans with at least 50% protein similarity. Four of the 33 loci are 99% identical to recent evolutionary duplications in a cluster of six potential rab loci in a small interval on the X chromosome at cytological location 9C–F, leading us to predict a total of 29 potential rab genes in Drosophila. We have recently performed a systematic profiling effort for 25 of these loci. The two other conserved loci in this X chromosomal cluster were the only predicted rab genes for which we found no expression. Hence, the total number of functional rab loci in Drosophila may only be 27. We have previously characterized 23 of these 27 through the analysis of rab-Gal4 driver lines. The Gal4/UAS system is the most widely used binary expression system in Drosophila. We used recombineering to precisely insert the Gal4 open reading frame into the start codon site of each rab GTPase within a large genomic fragment.