Slow-wave sleep and molecular chaperones

Since long ago, one of the most vital issues mankind is concerned about is why spending almost one-third of human lives for sleep. This review addresses the major function of slow-wave sleep (SWS) and molecular mechanisms of its regulation. The main conclusions are presented below as the following generalizations and hypotheses. 1. SWS performs an energy-conserving function which developed parallel to the evolution of tachimetabolism and endothermy/homoiothermy. 2. Most significant reduction in the brain energy demands during deep SWS, characterized by increased EEG delta power, creates optimal conditions for the enhancement of anabolic processes and actualization of the major biological function of sleep-accelerating protein synthesis in the brain. 3. Conditions of paradoxical sleep (PS) as an "archeowakefulness", containing the elements of endogenous stress, seem acceptable for chaperone expression required to fix misfolded proteins synthesized de novo during deep SWS. 4. Close integration of the HSP70 and HSP40 molecular systems, contained in the sleep center of the preoptic area of the hypothalamus, and their compensatory interrelationship contribute significantly to the maintenance of sleep homeostasis and implementation of its functions under non-stress conditions and during a long-term chaperone deficiency intrinsic to ageing and varied neuropathologies. 5. Cyclic changes in the protein synthesis rate (during deep SWS) and HSP70 chaperone expression (during wakefulness and, probably, PS), which occur on a daily basis throughout the entire lifetime, are critical for all vital functions of homeothermic organisms, including recovery of the nervous system structure and functions.