Deep sleep and anesthesia have contrasting effects on memory , yet at the microscopic scale they appear to produce similar neural network dynamics consisting of slow waves associated with alternating transients of high activity (UP states ) and silence (DOWN states) . Here, UP and DOWN state dynamics are analyzed in cortical recordings from human, monkey, and rat and found to be robustly different between deep sleep and anesthesia. We found that the temporal statistics of UP and DOWN states is robustly different in natural slow-wave sleep compared to the slow-waves of anesthesia. Computational models predict that an interplay between noise and spike-frequency adaptation can yield a transition from sleep-like to anesthesia-like slow-wave dynamics. These predictions were confirmed by pharmacological manipulations in vitro , inducing a switch between the two types of slow-waves. The results show that the strong adaptation found in anesthesia, but not in sleep, can produce a different type of slow oscillations, less sensitive to external inputs, that may prevent memory formation .
Sleep slow waves are known to participate in memory consolidation, yet slow waves occurring under anesthetized states 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 of slow waves is seen during sleep, while the second type prevails in anesthetized states. 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 .
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Deep sleep and anesthesia have contrasting effects on memory , yet at the microscopic scale they appear to produce similar neural network dynamics consisting of slow waves associated with alternating transients of high activity (UP states ) and silence (DOWN states)
Sleep slow waves are known to participate in memory consolidation, yet slow waves occurring under anesthetized states present no positive effects on memory
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UP and DOWN state dynamics are analyzed in cortical recordings from human, monkey, and rat and found to be robustly different between deep sleep and anesthesia. We found that the temporal statistics of UP and DOWN states is robustly different in natural
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
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sleep compared to the slow-waves of anesthesia. Computational models predict that an interplay between noise and
events. The first type of slow waves is seen during sleep, while the second type prevails in anesthetized states. 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
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can yield a transition from sleep-like to anesthesia-like slow-wave dynamics. These predictions were confirmed by pharmacological manipulations in vitro , inducing a
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
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slow-waves. The results
slow waves. Finally, we
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strong adaptation found in anesthesia, but not in sleep, can produce a different type of slow oscillations, less
first type of slow-wave dynamics is more
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inputs, that may prevent memory formation
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