In the postnatal brain, new neurons are continuously generated in the ventricular-subventricular zone and migrate toward the olfactory bulbs (OB), a primary center for olfactory processing. In the OB, each new neuron is differentiated into one of two types of olfactory interneurons, granule cell and periglomerular cell, located in the granule cell layer (GCL) and glomerular layer (GL), respectively. Here we report that the Sema3E-PlexinD1 signaling plays a critical role in the maintenance of neuronal migration in the OB. We found that granule cells form "lateral processes" branched from the leading process before the termination of their migration in the GCL, while periglomerular cells maintain their bipolar morphology until they stop their migration at the GL. PlexinD1 expression is maintained in the bipolar-shaped migrating neurons, but downregulated by endocytosis in the lateral-process-bearing cells before their termination of migration. In vitro FRET and photoactivation experiments revealed that Sema3E-PlexinD1 signaling decreases Rac1 activity, thereby suppressing formation of lateral processes, leading to the maintenance of bipolar migratory morphology of new neurons. PlexinD1 expression in migrating new neurons regulates their migration and final positioning within the OB, which is affected by odor enrichment. Taken together, results suggest that maintenance and termination of migration of new neurons by Sema3E-PlexinD1 signaling determines their final destination layers in the OB in an activity-dependent manner.