Search

Total sleep deprivation (TSD) of rats for 24 hours or less by continually enforced locomotion has consistently produced subsequent rebounds of slow-wave or high-amplitude EEG activity in NREM sleep, which has contributed to the widely held view that this EEG activity reflects particularly "intense" or restorative sleep. These rebounds usually have been accompanied by substantial rebounds of REM sleep. In contrast, chronic TSD (2 weeks or longer) by the disk-over-water (DOW) method has produced only huge, long-lasting rebounds of REM sleep with no rebound of high-amplitude NREM sleep. To evaluate whether the different rebounds result from different methods or from different lengths of deprivation, rats were subjected to 24-hour TSD by the DOW method. Rebounds included increases in high-amplitude and slow-wave activity; i.e., the methods produced similar rebound patterns following short-term TSD. (Chronic TSD by continually enforced locomotion would be strategically difficult and severely confounded with motor fatigue.) Rats subjected to DOW-TSD for 4 days, well before the development of severe TSD symptoms, showed primarily REM sleep rebounds. Rats subjected to 1 day of selective REM sleep deprivation, but not their closely yoked control rats, showed large, significant REM sleep rebounds, which evidently were not induced by the stress of the deprivation method per se. The combined findings prompted reexamination of published evidence relevant to "sleep intensity," including "negative rebounds," rebounds in other species, the effects of stress and fatigue, depth of sleep indicators, and extended sleep. The review points out pitfalls in the designation of any specific pattern as intense sleep.

Previous studies have demonstrated that albino but not pigmented rats show acute increases in REM sleep following light-to-dark transitions. Light and dark have also been shown to have direct effects on NREM sleep and wakefulness in albino rats. Little is known, however, about the direct light-dark effects on sleep patterns in pigmented animals. The purpose of the present study was to compare the direct effects of light and dark on REM sleep, NREM sleep, and waking in albino Lewis and pigmented Brown Norway (BN) rats.

Recent reports have indicated that rats subjected to total sleep deprivation (TSD) by the disk-over-water method and sacrificed when death appeared imminent showed aerobic bacteria in their blood. Yoked control rats did not. Extrapolating from these results, it has been suggested that the late body temperature declines and eventual deaths of TSD rats are caused by septicemia, and that other, earlier-appearing effects of TSD-including weight loss, increased energy expenditure, and regulation of temperature at a higher level-might be mediated by impaired host defenses against bacterial invasion. Three measures of aerobic bacterial invasion were used to evaluate these hypotheses: bacteremia, bacterial colonization in major organs of filtration (liver, kidney, and mesenteric lymph nodes), and adherence of bacteria to the cecal wall. Experiment 1 showed nonsignificant trends toward more bacterial invasion in 4-day TSD rats compared to yoked control rats and no relationship between the bacterial indicators and the early TSD effects. Experiment 2 showed that the elimination of aerobic bacterial infection by antibiotic treatment did not prevent the early TSD effects in 4-day TSD rats. Experiment 3 showed that the elimination of aerobic bacterial invasion in TSD rats did not eliminate the late temperature decline or the progression towards death. The results showed no significant evidence of aerobic bacterial invasion early in TSD and no indication that the major effects of TSD were dependent upon aerobic bacterial invasion.

Several letters to the editor are presented in response to articles in previous issues including "Vagaries of the Left," by John Zerzan in the Spring 2012 issue, "Dissent," by Paul J. Comeau in the Summer 2012 issue, and the drawing of a man named Coyote in the final page of the Spring 2012 issue.

TO THE EDITOR. —In discussing the pathologic changes in eyes of children who died after suspected child abuse, Elner et al1 asserted "that such trauma may be repeated is indicated by positive stains for hemosiderin"; this statement provides an opportunity for medicolegal confusion and miscarriage of justice. According to one source,2 hemosiderin, a breakdown product of hemoglobin from red blood cells, may be identified as early as 1 day after injury, although other authors3 are fairly circumspect and suggest that an interval of "several days" must pass before hemosiderin is deposited; macrophages that assemble ferritin into hemosiderin are identified at injury sites within 48 to 72 hours.Certainly, the detection of hemosiderin may indicate repeated trauma, but hemosiderin may also be a marker of survival after one episode of trauma. A child may be traumatized once and survive long enough for hemoglobin to be metabolized into hemosiderin.