  Sleep slow waves are known to participate in memory consolidation, yet slow
waves occurring under anesthesia present no positive effects on memory. Here,
we shed light onto this paradox, based on a combination of extracellular
recordings in vivo, in vitro, and computational models. We find two types of
slow waves, based on analyzing the temporal patterns of successive slow-wave
events. The first type is consistently observed in natural slow-wave sleep,
while the second is shown to be ubiquitous under anesthesia. Network models of
spiking neurons predict that the two slow wave types emerge due to a different
gain on inhibitory vs excitatory cells and that different levels of
spike-frequency adaptation in excitatory cells can account for dynamical
distinctions between the two types. This prediction was tested in vitro by
varying adaptation strength using an agonist of acetylcholine receptors, which
demonstrated a neuromodulatory switch between the two types of slow waves.
Finally, we show that the first type of slow-wave dynamics is more sensitive to
external stimuli, which can explain how slow waves in sleep and anesthesia
differentially affect memory consolidation, as well as provide a link between
slow-wave dynamics and memory diseases.
