IntroductionSleep is defined as a natural and reversible state of reduced reactivity to external stimuli and relative inactivity, accompanied by a loss of consciousness1. This inactive state has been evolutionarily conserved across species against many selective pressures. This suggests that sleep serves a vital function. Numerous studies have suggested that sleep improves both declarative and procedural memory 2,3. Consequently, memory consolidation is one of the apparent functions of sleep. The active system consolidation hypothesis and the synaptic homeostasis hypothesis (SHY) are the two main hypotheses for this putative function of sleep. The active system consolidation model proposes that repeated reactivation of new representations encoded in the hippocampus during slow-wave sleep (SWS) drives a transfer of memory traces from short-term memory in the hippocampus to neocortical regions for storage at long term4. These representations are stabilized in the neocortex during subsequent periods of REM sleep via synaptic potentiation5. SHY proposes that sleep acts to homeostatically renormalize synaptic weight to counteract the potentiation that occurs during wakefulness6,7. This occurs via an activity-dependent scaling of synaptic weight during SWS. These models are often depicted in direct opposition, largely due to the active enhancement proposed in the system's active consolidation model, as opposed to the global scaling (depowering) of SHY. However, it has recently been considered that these two models may not be mutually exclusive, but may act in unison8. This essay will analyze what I believe is the best evidence for and against each model to challenge the role of sleep in memory consolidation. The scroll ...... in the center of the paper ...... urated during the previous vigil. Napping studies show that SWA improves the ability to encode declarative memories47. The main function of the SHY is the reduction of energy consumption, once an unsustainable enhancement threshold has been reached. Further investigations will be needed to clarify the true role of sleep in memory consolidation. Over the past 10 years, a large amount of evidence has been produced to support the SHY theory. Now it is necessary to move on to the study of the underlying mechanisms. Altering the expression of LTP-associated genes or optogeneticly altering the input to specific cells at different sleep stages would provide a deeper understanding of the relationship between potentiation and SWS homeostasis. High-resolution monitoring of specific synapses during wakefulness and sleep would allow maximal assessment of SHY.