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In the rat, paradoxical sleep (PS) is preceded by a short-lasting stage characterized by high amplitude cortical spindles and low frequency hippocampal theta rhythm. This intermediate stage (IS) is massively extended at the expense of PS by barbiturates and benzodiazepines. To further study the relationship between the IS and PS, six rats were PS deprived for 48 h by sitting on one of three small platforms surrounded by water. A control group of six other rats remained in dry cages with shavings. After 24 h PS deprivation the latency of IS occurrence increased, was unchanged after 48 h deprivation and decreased during recovery on shavings after 52 h deprivation. The total IS duration, number of episodes and mean duration per episode were unchanged during deprivation but increased during recovery. This recovery was characterized by an increase in the number of PS episodes and the total duration while the latency of PS occurrence decreased. The frequency of theta rhythm, unchanged for PS, increased for the IS during deprivation and recovery. In conclusion, the IS did not substitute for PS after selective deprivation.

The effects of diazepam, a long half-life benzodiazepine, midazolam and triazolam, two with short half-life, on the transitional stage between deep slow wave sleep and paradoxical sleep were studied in Wistar and WAG/Rij rats. This intermediate stage is characterized by the unusual association of cortical spindles and low frequency hippocampal theta rhythm. The main result was extension of the intermediate stage at the expense of paradoxical sleep by diazepam and triazolam by influencing only the duration of the intermediate stage and both the onset and maintenance of paradoxical sleep. Midazolam increased both intermediate stage and paradoxical sleep. Several differences in the qualitative modulation of the stage characteristics and between rat strains were found. In regard to the possible peculiar physiological significance of the intermediate stage, we conclude that benzodiazepines promote a transient pharmacological cerveau isolé-like stage during sleep in rats.

Paradoxical sleep (PS) in mice, rats, and cats is preceded and sometimes followed by a short-lasting stage characterized by cortical high-amplitude spindles and hippocampal low-frequency theta rhythm. This intermediate stage (IS) seems to correspond to a transient functional disconnection of the forebrain from the brainstem. Pentobarbital and benzodiazepines greatly extend IS at the expense of PS, which is suppressed. Zolpidem, a new imidazopyridine hypnotic, was studied at 2.5, 5, and 7.5 mg/kg IP. At 2.5 mg/kg, which is already a true hypnotic dose, it only decreased PS during the first 2 h of recording with a rebound during the following 4 h of recording. At 5 mg/kg, zolpidem increased the number and total duration of IS episodes, increased IS episodes not followed by PS, and increased PS latency of occurrence. PS amount was decreased during the first three h with a rebound in the next 3 h. At 7.5 mg/kg, the total amount of PS was also decreased. The eye movement number and theta rhythm frequency of PS were unchanged. These results show that zolpidem produces less disruption of the association between IS and PS than do previous hypnotics.

Ritanserin, a 5-HT2 receptor antagonist, was injected intraperitoneally to rats at light onset. It was found that 0.63 mg/kg decreased waking, increased the slow waves characteristic of the first stage of sleep, and decreased paradoxical sleep (PS) during the first four hours. Active waking was further decreased and slow wave stage increased during the following four hours. The number of synchronized and paradoxical sleep phases decreased whereas their duration increased during the first four hours. Ritanserin at 2.5 mg/kg decreased active waking and PS, whereas quite waking and slow wave stage were increased during the first four hours. Quiet waking was increased during the following four hours. It is concluded that serotonin acting on 5 HT2 receptors is actively involved in sleep-waking regulation.

The aim of this investigation was to study ways of inducing prolonged contingent negative variations (CNV) in human subjects. Fourteen subjects underwent the following experimental procedure: 1st day: 2 CNVs in control conditions were recorded (16 successive trials, each with standard S1--S2 paradigm). 2nd day: 5 successive CNVs were recorded:(1) control; (2) labyrinthine stimulation before 1st, 5th, 9th and 13th trials with simple mental calculation performed between S1 and S2, i.e. during CNV; (3) mental calculation only; (4) labyrinthine stimulation only; (5) control. None of the three interference situations caused any significant changes in the mean and maximal CNV amplitudes measured between S1 and S2. On the other hand, the post-imperative part of the CNV was significantly (P less than 0.025) prolonged but only in the situation where 2 types of interference were applied at the same time. This increase disappeared with removal of the double interference. This change, which matches that observed spontaneously and reversibly in certain mental patients in the acute phase of their illness, seems to reflect a transient alteration of the psychophysiological state of the subject. The possibility of inducing these changes in a normal subject could serve as a means of determining the individual threshold of stress.

The positive components 1 and 2 of the averaged field response induced in the somesthetic S1 cortex by submaximal stimulation of cortical radiation and supramaximal stimulation of lemniscus medialis showed non-existent amplitude variability whereas the dispersion was significant for components 3, 4 and 5. The same stimulus delivered at a short intershock interval only induced waves 1 and 2 without any amplitude variability, the three following ones being under complete refractoriness. These results suggest a presynaptic origin of component 2.