“Sleep Deprivation in the Rat: An Update of the 1989 Paper”, 2002 (; backlinks):
[The reprinted report listed several major sleep deprivation effects which were apparent in all rats subjected to prolonged total sleep deprivation or paradoxical sleep deprivation by the disk-over-water method. Original effects that were confirmed in subsequent studies are listed.]
The reprinted report listed several major sleep deprivation effects (SDEs) which were apparent in all rats subjected to prolonged total sleep deprivation (TSD) or paradoxical sleep deprivation (PSD) by the disk-over-water (DOW) method. The following original effects were confirmed in subsequent studies:
Mortality: Unless deprivation was halted, all TSD rats died or showed signs of impending death—usually in about 2–3 weeks.2–10 The deaths (after about 4–6 weeks) of PSD rats were also confirmed.11,12
TSD and PSD rats lost weight in spite of increased food intake. The large rise in energy expenditure (EE, calculated from the caloric values of food intake and weight loss) was confirmed.2,4–9,13–17
The development of scrawny, debilitated appearance was confirmed.2,4–7,11
The severe ulcerative and hyperkeratotic skin lesions localized to the paws and tails of TSD and PSD rats were confirmed.2,4–7,9,11
As in the original studies, TSD rats showed an initial rise and subsequent decline in waking intraperitoneal temperature (Tip).2,4,5,10,11,14,16 As before, PSD rats showed only the Tip decline.11,12
As in the earlier report, recovery from extended TSD featured large rebounds of PS.6,16 Recent studies showed a predominance of PS rebound after only two18 or 419 days of TSD. Altogether, the confirmatory studies showed that TSD and PSD produce a reliably elicited syndrome of major biological effects.
…We think that the major impacts of our DOW sleep deprivation studies have been the demonstration by controlled experiments that, at least in the rat, sleep and paradoxical sleep are biological necessities and that extended sleep loss reliably produces a syndrome of specific, substantial physiological changes. Certainly, we did not discover anywhere near as much as we would have liked about why sleep is necessary. The deaths of the sleep deprived rats were the most dramatic consequences of sleep deprivation, but since death per se is such a nonspecific symptom, and since we did not find an unambiguous cause of death, that dramatic symptom did not tell us much about why sleep was necessary. Perhaps the most promising leads to functional importance are the 3 thermoregulatory failures. They are large, reliably elicited, functionally important changes worthy of further study. We have no clear idea of how that search should be pursued. Ideally, it would be interesting to record individual thermoregulatory neurons and observe how their spontaneous and responsive firing patterns change with sleep and extended sleep deprivation. A major problem would be how to hold such neurons over a long course of sleep deprivation.
Thus far, we have not had much success in deciphering how the thermoregulatory effects of sleep loss are mediated. Similarly, the cause of death, the deterioration of appearance, the skin lesions, and how brain activity is changed have resisted explication. As unlikely as it might seem, perhaps the problem is that the mediation might be related to functionally important physiological processes that have not yet been clearly identified—and that may be why the function of sleep has itself been such a tough nut to crack.50
.
See Also: