In parallel to this homeostatic process, sleep has been shown to contribute to memory consolidation. Notably, repeated reactivation of activity

patterns evoked during learning has been observed during slow-wave sleep both in rats and humans. This reactivation of memory traces (“replay”), which correlate with memory consolidation, may redistribute the neural representations of memory into cortical regions for long-term storage (Diekelmann and Born, 2010). With all these important functions, sleep is no longer considered a passive resting state, but rather an active brain state essential for neuronal plasticity. In this issue of Neuron, Yokoyama et al. (2011) report exciting data extending this concept from synapses to neural circuits, illustrating an unexpected function MK-1775 molecular weight of sleep in rescaling the number of neurons in the olfactory bulb

(OB). In the OB, the first central relay of the olfactory system, adult neurogenesis provides a continuous source of new neurons that mature and integrate into the preexisting OB network to become mainly mature GABAergic granule cells. Alongside this integration is a selection Tanespimycin concentration process in which 50% of the new neurons undergo apoptosis during a specific critical window ( Yamaguchi and Mori, 2005). How this selection process is regulated is the focus of intense study. In this paper, the authors discovered that a food restriction paradigm exerts a peculiar effect on apoptosis of newborn cells. They first observed that while the degree of apoptosis is constant over time in mice Ketanserin allowed unlimited access to food, the number of apoptotic neurons increases strongly after eating when food is formerly and briefly restricted (for 4 hr). Interestingly, most of the apoptotic neurons were newly formed granule cells, confirming that the newborn neuron population is in constant turnover. More puzzling was the time course of this phenomenon: apoptosis approximately doubled two hours after animals begin eating. But food was not the only factor regulating cell death. Apoptosis was

potentiated only when animals underwent a postprandial nap, and this correlated with postprandial sleep duration. When animals were selectively sleep deprived after eating, apoptosis was prevented. This phenomenon was also seen to a lesser extent in ad libitum feeding mice when the authors carefully monitored feeding and postprandial behaviors for each individual. By showing that the degree of apoptosis enhancement remains constant at different circadian times, the authors also ruled out potential circadian influences in this phenomenon. What is the importance of sensory experience to this process? The OB is a great model to test experience-dependent phenomena since the sensory inputs can be easily manipulated and this manipulation can be restricted to one region of the OB, leaving other inputs intact. The authors used two strategies to reduce olfactory activity.