1. Sixteen rats were recorded continuously for 3 days using an automated system that detected, quantified, and stored the incidence of cortical delta waves, cortical sigma spindles, hippocampal theta rhythm, and electromyographic activity. A time series then was constructed wherein 15-s epochs were ascribed to one behavioral state: wakefulness (W), quiet sleep (QS), or active sleep (AS, a state also referred to as REM sleep). From those series, AS episodes and non-AS intervals could be determined. Episodes and intervals were defined as lasting at least two epochs and the one-epoch episodes and intervals were incorporated to the ongoing state. 2. Having established the length of each AS episode and non-AS interval, pairings were made, on the one hand between episodes and their preceding intervals, and on the other, between episodes and the intervals that followed. 3. Highly significant correlations were found between the length of AS episodes and the length of the non-AS intervals that followed. Correlations were also significant when calculated separately versus the amount of QS and of W within the following interval. Correlations improved when they were performed against the log of the interval and when only intervals with a predominance of QS were selected. 4. No significant correlation was found between the length of AS episodes and the length of the preceding non-AS intervals, except for a negative one that was present only when the statistical analysis was performed in the unsmoothed array where the one-epoch episodes and intervals were preserved. 5. These results suggest that there is a short-term homeostasis operating within the spontaneous architecture of sleep in rats. This homeostatic mechanism is not manifested by the regulation of the length of AS episodes. Instead, there is a forward regulatory mechanism that, given the duration of an AS episode, permissively controls the interval that the animal may abstain from AS, and hence the timing of the triggering of a new AS episode.

During specific rapid eye movement (REM) sleep deprivation its homeostatic regulation is expressed by progressively more frequent attempts to enter REM and by a compensatory rebound after the deprivation ends. The buildup of pressure to enter REM may be hypothesized to depend just on the time elapsed without REM or to be differentially related to non-REM (NREM) and wakefulness. This problem bears direct implications on the issue of the function of REM and its relation to NREM. We compared three protocols that combined REM-specific and total sleep deprivation so that animals underwent similar 3-h REM deprivations but different concomitant NREM deprivations for the first 2 (2T1R), 1 (1T2R), or 0 (3R) hours. Deprivation periods started at hour 6 after lights on. Twenty-two chronically implanted rats were recorded. The median amount of REM during all three protocols was approximately 1 min. The deficits of median amount of NREM in minutes within the 3-h deprivation periods as compared with their baselines were, respectively for 2T1R, 1T2R, and 3R, 35 (43%), 25 (25%), and 7 (7%). Medians of REM rebound in the three succeeding hours, in minutes above baseline, were, respectively, 8 (44%), 9 (53%), and 9 (50%), showing no significant differences among protocols. Attempted transitions to REM showed a rising trend during REM deprivations reaching a final value that did not differ significantly among the three protocols. These results support the hypothesis that the build up of REM pressure and its subsequent rebound is primarily related to REM absence independent of the presence of NREM.

Isogenic Escherichia coli strains, differing in their expression of K1 antigen and ColV plasmid, were studied for their ability to produce disease. Newborn rats were used to test the ability of these strains to colonize the intestine and to produce bacteremia and meningitis; adult rats were used to test their ability to produce urinary tract infection. Colonization of intestine and bladder by K1+ ColV+ E. coli was associated with rapid induction of bacteremia and higher mortalities compared with colonization with K1+ ColV- strains. These findings suggest that the ColV plasmid could play a role in the pathogenesis of human infections.

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