The role of adult hippocampal neurogenesis in spatial learning remains a matter of debate. Here, we show that spatial learning modifies neurogenesis by inducing a cascade of events that resembles the selective stabilization process characterizing development. Learning promotes survival of relatively mature neurons, apoptosis of more immature cells, and finally, proliferation of neural precursors. These are three interrelated events mediating learning. Thus, blocking apoptosis impairs memory and inhibits learning-induced cell survival and cell proliferation. In conclusion, during learning, similar to the selective stabilization process, neuronal networks are sculpted by a tightly regulated selection and suppression of different populations of newly born neurons.

Neurogenesis in the hippocampus is characterized by the birth of thousand of cells that generate neurons throughout life. The fate of these adult newborn neurons depends on life experiences. In particular, spatial learning promotes the survival and death of new neurons. Whether learning influences the development of the dendritic tree of the surviving neurons (a key parameter for synaptic integration and signal processing) is unknown. Here we show that learning accelerates the maturation of their dendritic trees and their integration into the hippocampal network. We demonstrate that these learning effects on dendritic arbors are homeostatically regulated, persist for several months, and are specific to neurons born during adulthood. Finally, we show that this dendritic shaping depends on the cognitive demand and relies on the activation of NMDA receptors. In the search for the structural changes underlying long-term memory, these findings lead to the conclusion that shaping neo-networks is important in forming spatial memories.adult neurogenesis | memory | spatial learning | hippocampus | dendrite I n the search for the mechanisms underlying long-term memory formation, structural changes have been proposed to play a major role (1). Adult neurogenesis, a novel form of structural plasticity, occurs in the dentate gyrus (DG), a key structure in processing spatial relational memory (2). Adult neurogenesis in the DG is a complex, multistep process that starts with the proliferation of neural precursors residing in the dentate subgranular layer (2). At least 50% of the daughter cells die within a few days after their birth. The adult-born cells that survive this initial period of cell death differentiate mainly into granule neurons. These new mature neurons are synaptically integrated into the dentate network, where they receive functional inputs (3) and form functional synapses with their target cells (4).Adult-born neurons contribute to the formation of memories, particularly spatial memory as measured in the water maze (5, 6). Reciprocally, spatial learning has been shown to influence adult neurogenesis (7). We have shown that during spatial learning and similar to the selective stabilization process observed during brain development, neuronal networks are sculpted by a tightly regulated selection and suppression of different populations of newly born neurons (8). This homeostatic regulation of the numbers of newly born neurons is important for spatial memory, because its alteration leads to memory deficits (8, 9).One of the requirements for the new neurons to process information is the development of extensive dendritic arbors capable of receiving and integrating complex spatiotemporal patterns of synaptic inputs (4). Whether learning influences such a dendritic development is unknown. To address this issue, we used doublecortin (Dcx) and retroviral labeling to examine to what extent spatial learning in the water maze affects the dendritic morphology of adult-born neurons. Furthermore, we investigated whether the ...