Restoration of Learning Capacity During Sleep
Restoring Synaptic Homeostasis During Sleep
Next to the idea of active system consolidation, the most influential theory of sleep’s function for memory is the synaptic homeostasis hypothesis. According to this hypothesis, the widespread synaptic potentiation occurring at encoding of information during wakefulness leads to increased demands of space and energy in the brain. If this development remained unchecked the brain would shortly reach the limits of its encoding and/or upkeep capabilities. Sleep is essential to renormalize synaptic weights (termed “synaptic downscaling”) and has therefore been suggested to be “the price we pay for plasticity”. Indeed, overall synaptic spines as well as markers for synaptic potentiation increase across periods of wakefulness and decrease during periods of sleep. Computer simulations have established the theoretical effectiveness of slow wave activity (0.5–4Hz) to renormalize synapses, and potentiating synapses by extended learning or by transcranial magnetic stimulation induces local increases of slow wave activity. Conversely, immobilizing a human’s arm reduces slow wave activity and slow wave sleep deprivation impairs visuo-motorlearning. In correspondence with the general finding that slow wave activity is homeostatic ally regulated this line of research in dicates that slow wave activity may play a major role for synaptic homeostasis. However, it has also been shown that learning increases sleep spindles, and since the synaptic homeostasis theory makes no explicit claims as to the specific mechanisms involved, their exact nature as well as their association with specific sleep stages remain to be determined.