Sleep states and sleep electroencephalographic spectral power in mice lacking the beta 3 subunit of the GABA(A) receptor

Mice lacking the GABA(A) receptor beta(3) subunit exhibit a profound disruption in thalamic circuitry. We have studied sleep in these mice under baseline conditions and following treatment with the benzodiazepine midazolam. Under baseline conditions, NREM sleep time did not differ between beta(3) subunit knockout mice and wild type mice, while REM sleep time was significantly lower in knockout mice than in wild type mice during the light portion of a 24-h light-dark cycle. In constant dark conditions, circadian rhythmicity remained intact in mutant mice for a period of at least 9 days. EEG delta power (1-4 Hz) was significantly greater in the knockout than in wild type mice during NREM sleep but not during other states. A transient increase in EEG power in the 12-16 Hz range that occurred in wild type mice just prior to the transition from NREM to REM sleep was present but significantly blunted in the knockout. Midazolam decreased NREM delta power and REM time in wild type mice. The former but not the latter response to midazolam was intact in the knockout. These results further support a role for GABAergic transmission in regulating REM sleep and EEG spectral phenomena associated with NREM sleep.     

Sigma (12-15 Hz) and delta (0.3-3 Hz) EEG oscillate reciprocally within NREM sleep

Sleep EEG in the sigma and delta frequency bands was subjected to spectral analysis in 8 normal young adults. In each subject, power density of sigma and delta oscillated reciprocally during NREM sleep, confirming an observation made initially with period/amplitude analysis. In REM sleep, power density for both frequency bands was at its lowest levels. Correlation coefficients between power density of delta vs. 1/sigma for all artifact-free 20-s epochs of NREM sleep/night were highly significant for each subject. These results show that cyclic oscillation of EEG within sleep is not limited to delta frequencies. The reciprocal relation of sigma to delta holds implications for the EEG mechanisms of NREM sleep. This dynamic pattern may also prove useful for sleep stage scoring and for a finer empirical analysis of sleep in psychiatric and neurological disorders.     

Periodic limb movements both in non-REM and REM sleep: Relationships between cerebral and autonomic activities

ObjectiveTo investigate the temporal relationship between cerebral and autonomic activities before and during periodic limb movements in NREM and REM sleep (PLMS).MethodsPatterns of EEG, cardiac and muscle activities associated with PLMS were drawn from polysomnographic recordings of 14 outpatients selected for the presence of PLMS both in NREM and REM sleep. PLMS were scored during all sleep stages from tibial EMG. Data from a bipolar EEG channel were analyzed by wavelet transform. Heart rate (HR) was evaluated from the electrocardiogram. EEG, HR and EMG activations were detected as transient increase of signal parameters and examined by analysis of variance and correlation analysis independently in NREM and REM sleep. Homologous parameters in REM and NREM sleep were compared by paired t-test.ResultsThe autonomic component, expressed by HR increase, took place before the motor phenomenon both in REM and NREM sleep, but it was significantly earlier during NREM. In NREM sleep, PLM onset was heralded by a significant activation of delta-EEG, followed by a progressive increase of all the other bands. No significant activations of delta EEG were found in REM sleep. HR and EEG activations positively correlated with high frequency EEG activations and negatively (in NREM) with slow frequency ones.ConclusionsOur findings suggested a heralding role for delta band only in NREM sleep and for HR during both NREM and REM sleep. Differences in EEG and HR activation between REM and NREM sleep and correlative data suggested a different modulation of the global arousal response.SignificanceIn this study, time–frequency analysis and advanced statistical methods enabled an accurate comparison between brain and autonomic changes associated to PLM in NREM and REM sleep providing indications about interaction between autonomic and slow and fast EEG components of arousal response.     

Sleep and sleep regulation in the ferret (Mustela putorius furo)

We investigated sleep-wake (S-W) architecture and sleep regulation in the ferret: a phylogenetically primitive mammal increasingly used in neurobiological studies. Twenty-four hour S-W baseline data were collected in eight adult ferrets. Seven ferrets were then sleep deprived for 6h at the beginning of the light period. Like other placental mammals, ferrets exhibited the main vigilance states of wakefulness, rapid-eye-movement (REM) sleep and non-REM (NREM) sleep. Interestingly, the amount of REM sleep in the ferret was considerably higher (24.01+/-1.61% of total recording time) than typically reported in placental mammals. Ferret sleep was homeostatically regulated as sleep deprivation produced a significant increase in NREM EEG delta power during the recovery period. Therefore, ferret sleep in most respects is comparable to sleep in other placental mammals. However, the large amount of REM sleep in this phylogenetically more ancient species suggests that REM sleep may have been present in greater amounts in early stages of mammalian evolution.     

Selective alterations of the first NREM sleep cycle in humans by a dopamine D1 receptor antagonist (NNC-687)

This paper details the first study of the effects of dopamine D1 receptor antagonism on the regulation of human sleep EEG (electroencephalogram). The investigational drug NNC-687 (NNC 01-0687/CEE 03-310) was administered to 20 healthy young men in doses of 5, 10, and 15 mg in a double blinded, placebo controlled, crossover design. In rats, dopamine D1 receptor antagonism can produce large increases in the amounts of both rapid eye-movement (REM) and non-rapid eye-movement (NREM) sleep. In this study, drug effects were most prominent in the first NREM period. D1 antagonism markedly reduced the peak-amplitude of delta EEG waves but increased their instantaneous frequency as well as enhancing the total number, incidence, and burst-duration of sleep spindles. The length of the first NREM period was increased up to 47% over baseline. Despite these large increases in NREM sleep time, the amount of delta EEG power accumulated over the first NREM period was conserved at baseline levels. We note that the sleep-EEG profile of D1 antagonism is very similar to that of GABAA (gamma-aminobutyric acid) receptor modulators and suggest that D1 antagonism may alter the properties of the neuronal networks which generate delta and spindle, and K-complex EEG waveforms through the upstream modulation of GABAA receptor activity.     

The sleep EEG's microstructure in depression: alterations of the phase relations between EEG rhythms during REM and NREM sleep

OBJECTIVE: We investigated the microstructure of sleep electroencephalograms (EEGs) of 13 unmedicated depressive inpatients and 13 healthy controls matched in sex and age, hypothesizing that depressives depict an alteration of certain EEG oscillations across the night. METHODS: We digitized the sleep EEGs with a sampling rate of 100 Hz (bipolar derivation C(z)-P(z), 1440 single sweeps; 2048 data points each), calculated the time course of delta (1-3.5 Hz), theta (3.5-7.5 Hz), alpha (7.5-15 Hz), and beta (15-35 Hz) activity over the night, and determined the correlation coefficients of these different EEG rhythms separately for rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. RESULTS: For both groups we detected a clear difference between REM and NREM sleep cycles at certain frequency bands. The most impressive changes occurred for the delta/beta and theta/beta correlations, which change their signs between NREM (negatively correlated) and REM (positively correlated) sleep cycles. Following an analysis of variance model with repeated measurement design, a statistically significant group effect (P=0.024) between depressives and controls was observable during NREM sleep for the delta/beta (P=0.010) and theta/beta (P=0.018) interactions. CONCLUSION: We detected alterations of certain sleep EEG oscillations during the NREM sleep cycle, where the delta/beta as well as the theta/beta activities were higher (negatively) compared to healthy controls. Together with previous investigations on the influence of antidepressants on the microstructure of sleep EEGs, this is another hint that the NREM sleep cycle plays a major role in depression.     

Design and validation of a computer-based sleep-scoring algorithm

A computer-based sleep scoring algorithm was devised for the real time scoring of sleep-wake state in Wistar rats. Electroencephalogram (EEG) amplitude (microV(rms)) was measured in the following frequency bands: delta (delta; 1.5-6 Hz), theta (Theta; 6-10 Hz), alpha (alpha; 10.5-15 Hz), beta (beta; 22-30 Hz), and gamma (gamma; 35-45 Hz). Electromyographic (EMG) signals (microV(rms)) were recorded from the levator auris longus (neck) muscle, as this yielded a significantly higher algorithm accuracy than the spinodeltoid (shoulder) or temporalis (head) muscle EMGs (ANOVA; P=0.009). Data were obtained using either tethers (n=10) or telemetry (n=4). We developed a simple three-step algorithm that categorizes behavioural state as wake, non-rapid eye movement (NREM) sleep, rapid eye movement (REM) sleep, based on thresholds set during a manually-scored 90-min preliminary recording. Behavioural state was assigned in 5-s epochs. EMG amplitude and ratios of EEG frequency band amplitudes were measured, and compared with empirical thresholds in each animal.STEP 1: EMG amplitude greater than threshold? Yes: "active" wake, no: sleep or "quiet" wake. STEP 2: EEG amplitude ratio (delta x alpha)/(beta x gamma) greater than threshold? Yes: NREM, no: REM or "quiet" wake. STEP 3: EEG amplitude ratio Theta(2)/(delta x alpha) greater than threshold? Yes: REM, no: "quiet" wake. The algorithm was validated with one, two and three steps. The overall accuracy in discriminating wake and sleep (NREM and REM combined) using step one alone was found to be 90.1%. Overall accuracy using the first two steps was found to be 87.5% in scoring wake, NREM and REM sleep. When all three steps were used, overall accuracy in scoring wake, NREM and REM sleep was determined to be 87.9%. All accuracies were derived from comparisons with unequivocally-scored epochs from four 90-min recordings as defined by an experienced human rater. The algorithms were as reliable as the agreement between three human scorers (88%).     

Sleep EEG in mice that are deficient in the potassium channel subunit K.v.3.2

Voltage-gated potassium channels containing the K.v.3.2 subunit are expressed in specific neuronal populations such as thalamocortical neurons and fast spiking GABAergic interneurons of the neocortex and hippocampus. These K(+)-channels play a major role in the regulation of firing properties in these neurons. We investigated whether the K.v.3.2 subunit contributes to the generation of the sleep electroencephalogram (EEG). The EEG of a frontal and occipital derivation of K.v.3.2-deficient mice and littermate controls was recorded during a 24-h baseline, 6-h sleep deprivation (SD) and subsequent 18-h recovery to assess also the effects of the K.v.3.2 subunit deficiency under physiological sleep pressure. The K.v.3.2-deficient mice had lower EEG power density in the frequencies between 3.25 and 6 Hz in nonREM (NREM) sleep and 3.25-5 Hz in REM sleep. These differences were more prominent in the frontal derivation than in the occipital derivation. The waking EEG spectrum was not affected by the deletion. In both genotypes SD induced a prominent increase in slow-wave activity in NREM sleep (mean EEG power density between 0.75 and 4.0 Hz), and a concomitant decrease in sleep fragmentation. The effects of SD did not differ significantly between the genotypes. The results indicate that K.v.3.2 channels may be involved in the generation of EEG oscillations in the high delta and low theta range in sleep. They support the notion that GABA-mediated synchronization of cortical activity contributes to the electroencephalogram.     

Influence of sleep stage and wakefulness on spectral EEG activity and heart rate variations around periodic leg movements.

OBJECTIVE: Typical changes in spectral electroencephalographic (EEG) activity and heart rate (HR) have been described in periodic leg movements (PLM) associated with or without microarousals (MA). We aimed to determine the effects of sleep stage and wakefulness on these responses to ascertain whether a common pattern of EEG and HR activation takes place. METHODS: The time course of EEG spectral activity and HR variability associated with PLM was analysed in 13 patients during light NREM sleep, rapid-eye-movement (REM) sleep and wakefulness. The same analysis was also conducted for PLM without MA occurring in stage 2. RESULTS: A significant EEG and electrocardiogram (ECG) activation was found associated with PLM during sleep, but not during wakefulness. While in light NREM sleep, an increase in delta and theta bands was detected before the PLM onset, in REM sleep the EEG activation occurred simultaneously with the PLM onset. Moreover, during stage 1 and REM sleep, alpha and fast frequencies tended to remain sustained after the PLM onset. In contrast, during wakefulness, a small and not significant increase in cerebral activity was present, starting at the PLM onset and persisting in the post-movement period. A typical pattern of cardiac response was present during NREM and REM sleep, the autonomic activation being lesser and prolonged during wakefulness. CONCLUSIONS: We conclude that the EEG and HR responses to PLM differ between sleep stages and wakefulness with lesser changes found during wakefulness. SIGNIFICANCE: These findings suggest that specific sleep state-dependent mechanisms may underlie the occurrence of PLM.     

Baseline and post-deprivation recovery sleep in SCN-lesioned rats

In humans, advancing age alters sleep patterns, reducing high voltage NREM sleep, sleep bout length, and delta power during NREM sleep. Although the mechanism by which these alterations occur is unknown, age-related changes in normal circadian processes may play a role. Increased age produces histological and functional changes in the suprachiasmatic nucleus (SCN), and alters the amplitude and phase of circadian rhythms. To examine the relationship between SCN function and age-related changes in sleep, we produced radiofrequency (RF) lesions of the SCN in rats of different ages and examined sleep behavior before and after sleep deprivation. Three-, 12- and 18-month-old rats received RF or sham lesions of the SCN. After verifying loss of circadian rhythm, 24-h EEG/EMG/temperature recordings were made in dim light before and after 24 h of sleep deprivation using the disk-over-water method. Age-related changes in NREM sleep, sleep bout length, and delta EEG power persisted despite SCN lesions. SCN lesions in all age groups increased baseline NREM sleep by 4% and NREM delta power by 15%, and decreased REM sleep by 10%. Although SCN lesions initially produced more REM and NREM sleep during recovery, 24-h values did not differ. Deteriorating SCN function is unlikely to cause the characteristic changes in sleep that occur with age. Our data also imply that an intact SCN slightly inhibits NREM sleep in the rat. Changes in NREM sleep and delta EEG power during recovery in lesioned rats suggest that the SCN may influence homeostatic regulation.     

Band-specific electroencephalogram and brain cooling abnormalities during NREM sleep in patients with winter depression.

BACKGROUND: We previously reported that delta wave activity and facial skin temperatures, an index of brain cooling activity, were both abnormal during sleep in patients with winter depression (SAD). Because other electroencephalographic (EEG) frequencies may also convey relevant thermal, homeostatic, and circadian information, we sought to spectrally analyze delta, theta, alpha, and sigma frequencies during sleep from 23 patients with SAD and 23 healthy control subjects. METHODS: We computed means for delta, theta, alpha, and sigma power during both NREM and REM sleep. We also generated 22 cross-correlation functions for each group by crossing facial and rectal temperature with each other, as well as with delta, theta, alpha, and sigma frequencies. RESULTS: We found that delta, theta, and alpha frequency activities were all increased during NREM, but not REM sleep, in patients with SAD. In addition, there were significant and abnormal cross-correlations between facial temperatures and delta and theta frequencies during NREM sleep in patients with SAD. CONCLUSIONS: Patients with winter depression exhibit correlated abnormalities of sleep homeostasis and brain cooling during NREM sleep. Their EEG profiles during NREM sleep resemble the EEG profiles of subjects who have been sleep deprived. Further studies of NREM sleep homeostasis in patients with SAD seem warranted.     

INFLUENCE OF AGE ON THE INTERRELATION BETWEEN EEG FREQUENCY BANDS DURING NREM AND REM SLEEP

The age-dependence of temporal interrelations between distinct frequency bands of sleep EEG was investigated in a group of 59 healthy young and middle-aged males via cross correlation analysis. Based on global evaluation throughout the entire night, a highly significant decline of the delta/theta correlation with increasing age was found. A separate analysis for non-rapid eye movement (NREM) and rapid eye movement (REM) sleep revealed different changes with aging. During NREM sleep, the correlation between the delta and theta frequency bands decreased with increasing age. In contrast, during REM sleep, a stronger correlation became obvious between the theta, alpha, and beta frequency bands with increasing age, whereas the lower frequency components were not affected. These findings indicate that aging processes seem to interact with sleep EEG rhythms in a complex manner, where most conspicuous is a disintegration of the activities in the lower frequency range, both concerning the successive sleep cycles across the night and the microstructure of NREM sleep     

Influence of age on the interrelation between EEG frequency bands during NREM and REM sleep

The age-dependence of temporal interrelations between distinct frequency bands of sleep EEG was investigated in a group of 59 healthy young and middle-aged males via cross correlation analysis. Based on global evaluation throughout the entire night, a highly significant decline of the delta/theta correlation with increasing age was found. A separate analysis for non-rapid eye movement (NREM) and rapid eye movement (REM) sleep revealed different changes with aging. During NREM sleep, the correlation between the delta and theta frequency bands decreased with increasing age. In contrast, during REM sleep, a stronger correlation became obvious between the theta, alpha, and beta frequency bands with increasing age, whereas the lower frequency components were not affected. These findings indicate that aging processes seem to interact with sleep EEG rhythms in a complex manner, where most conspicuous is a disintegration of the activities in the lower frequency range, both concerning the successive sleep cycles across the night and the micro-structure of NREM sleep.     

The impact of chronic primary insomnia on the heart rate – EEG variability link

ObjectiveTo determine if chronic insomnia alters the relationship between heart rate variability and delta sleep determined at the EEG.MethodsAfter one night of accommodation, polysomnography was performed in 14 male patients with chronic primary insomnia matched with 14 healthy men. ECG and EEG recordings allowed the determination of High Frequency (HF) power of RR-interval and delta sleep EEG power across the first three Non Rapid Eye Movement (NREM)–REM cycles. Interaction between normalized HF RR-interval variability and normalized delta sleep EEG power was studied by coherency analysis.ResultsPatients showed increased total number of awakenings, longer sleep latency and wake durations and shorter sleep efficiency and REM duration than controls (p < .01). Heart rate variability across first three NREM–REM cycles and sleep stages (NREM, REM and awake) were similar between both groups. In each group, normalized HF variability of RR-interval decreased from NREM to both REM and awake. Patients showed decreased linear relationship between normalized HF RR-interval variability and delta EEG power, expressed by decreased coherence, in comparison to controls (p < .05). Gain and phase shift between these signals were similar between both groups.ConclusionsInteraction between changes in cardiac autonomic activity and delta power is altered in chronic primary insomniac patients, even in the absence of modifications in heart rate variability and cardiovascular diseases.SignificanceThis altered interaction could reflect the first step to cardiovascular disorders.     

Effects of social stimuli on sleep in mice: non-rapid-eye-movement (NREM) sleep is promoted by aggressive interaction but not by sexual interaction

Sleep is generally considered to be a process of recovery from prior wakefulness. In addition to being affected by the duration of the waking period, sleep architecture and sleep EEG also depend on the quality of wakefulness. In the present experiment, we examined how sleep is affected by different social stimuli (social conflict and sexual interaction). Male C57BL/6J mice were placed in the cage of an aggressive dominant male or an estrous female for 1 h in the middle of the light phase. The conflict with an aggressive male had a pronounced NREM sleep-promoting effect. EEG slow wave activity, a measure of NREM sleep intensity, was increased for about 6 h and NREM sleep time was significantly increased for 12 h. REM sleep was strongly suppressed during the remainder of the light phase after the conflict, followed by a rebound later in the recovery phase. The sexual interaction, in contrast, had only mild effects. Both NREM sleep and REM sleep were somewhat suppressed shortly after the interaction. In a separate group of mice, blood samples were taken to measure prolactin and corticosterone. The results suggest that the temporary suppression of REM sleep following the social stimuli may be partly due to elevated corticosterone. The different effects of the social stimuli on NREM sleep are not easily explained by differences in the hormone responses. In conclusion, although both social conflict and sexual interaction induce a strong physiological activation, only social conflict has a strong stimulatory effect on NREM sleep mechanisms.     

EEG sleep in young depressives: first and second night effects

The sleep electroencephalogram (EEG) of young, drug-free, recurrently depressed outpatients was analyzed for 2 nights and was compared to age-matched controls using a variety of standard and computerized measures of sleep activity. On the first night, young depressives showed significantly greater difficulty in falling asleep and decreased sleep efficiency. Sleep architecture differences between the young depressives and controls were highlighted by increased percentages of Stage 2 sleep and major decreases in Stages 3 and 4 (delta wave) sleep among the depressives, as indicated by either period analyses or spectral analysis. The greatest differences in delta wave activity during night 1 were found in the first two (non-rapid eye movement (NREM) periods as measured by period analysis (NREM period 1, p less than 0.04; NREM period 2, p less than 0.001--average delta wave count) or by spectral analysis for the first 100 min of sleep (0.5-2.0 Hz). In contrast to the NREM sleep findings, various REM variables, including REM latency did not significantly distinguish the two subject groups for either night 1 or 2. Stepwise discriminant analysis demonstrated that night 1 sleep latency and delta wave counts during the second NREM period correctly classified 100% of all 16 individuals studied. The only differences between the young depressed patients and controls that remained on night 2 were significant reductions in slow-wave sleep as quantified by the computerized methods. Taken together, these findings suggest that the EEG response of young outpatients to the first night's stay in a sleep laboratory may be a useful tool for the diagnosis of depression in this age group. In addition, the use of computerized methods in this study point to an underlying deficit in delta sleep waveforms as being a prominent feature of the sleep of young depressed subjects.     

Effects of tetrodotoxin (TTX) inactivation of the central nucleus of the amygdala (CNA) on dark period sleep and activity

The amygdala has been implicated in emotional arousal and in the regulation of sleep. Previously, we demonstrated that tetrodotoxin (TTX), a sodium channel blocker that temporarily inactivates neurons and tracts, microinjected into the central nucleus of the amygdala (CNA) during the light period significantly reduced REM, shortened sleep latency, and increased EEG delta power in rats. TTX inactivation of CNA also reduced activity in the open field. These findings suggest that the amygdala modulates arousal in a variety of situations. To test the hypothesis that the amygdala may influence spontaneous arousal, we examined the effects of TTX inactivation of CNA on sleep and activity during the dark period when rats show higher arousal and less sleep. EEG and activity were recorded via telemetry in Wistar rats (n = 8). Bilateral microinjections of TTX (L: 2.5 ng/0.1; H: 5.0 ng/0.2 microl) or SAL (saline, 0.2 microl) were administered before lights off followed by recording throughout the 12-h dark period and following 12-h light period. Microinjections were given at 5-day intervals and were counterbalanced across condition. TTX significantly shortened sleep latency, increased NREM time, decreased REM time, and decreased activity. TTX increased NREM episode duration, whereas the number and duration of REM episodes were decreased. The present results indicate that TTX inactivation of CNA can increase NREM time when spontaneous arousal is high, suggesting a broad role for the amygdala in regulating arousal. The results suggest that understanding the ways in which the amygdala modulates arousal may provide insight into the mechanisms underlying altered sleep in mood and anxiety disorders.     

Nocturnal sleep in infants with congenital cerebral malformation

Sleep EEG patterns in 17 infants with cerebral malformations (4 months to 4 years of age) were studied throughout nocturnal sleep and the following results were obtained. Seven cases evidenced normal sleep/wakefulness EEG patterns that could be classified into 6 stages. Ten cases showed abnormal sleep EEG patterns as follows: absence of sleep spindles (n = 7) which included cases of absence of EEG patterns characteristic of wakefulness, NREM sleep and REM sleep (n = 5), no characteristic EEG patterns of stages 1-4 (n = 1) and stages W, 1, 2 and REM (n = 1) and the remaining cases with absence of spindles (n = 1), and spindles with an extremely low incidence (n = 2). Short sleep and long awaking times, and no delta rhythmicity during the night, were noted in 5 out of 17 subjects. A significant decrease of DQ was found in subjects with indistinguishable stages including stages W, 1, 2 and REM, as compared with those patients whose stages were all distinguishable.     

Polysomnographic quantification of bioelectrical maturation in preterm and fullterm newborns at matched conceptional ages

We analyzed the relationship between normal neonatal EEG features and gestational age and conceptional age, and evaluated the normal aspects of EEG maturation in preterm babies compared to term babies. We report 46 newborns, divided into two groups. Group I consisted of 11 newborns with gestational age between 30 and 32 weeks, followed with weekly polysomnograms until they reach 42 weeks' conceptional age. Group II (control) consisted of 35 newborns with gestational ages of 34 weeks (n = 5), 36 weeks (n = 10), 38 weeks (n = 10) and 40 weeks (n = 10) evaluated with one polysomnogram in their first 24–48 h of life. In each examination one 5 min epoch in REM and NREM sleep was analyzed to quantify the number of delta brushes, the presence of frontal and temporal sharp transients, the presence of delta frontal rhythmic activity, the grade of concordance between EEG patterns and sleep stages, the percent of interhemispheric synchrony and the duration of interburst interval. The age dependent variability of the EEG patterns was evaluated during the subsequent weeks with group comparisons at weeks 34, 36, 38 and 40. Our results show that the number of delta brushes and the duration of the interburst interval decrease as gestational and conceptional age increase. The percent of interhemispheric synchrony increases with gestational and conceptional age. The presence of frontal sharp transients and delta frontal rhythmic activity suggest that the newborn is fullterm. The presence of temporal sharp transients suggest a preterm newborn. The degree of concordance between behavioral sleep patterns and EEG was more helpful in recognizing sleep stages than in estimating gestational or conceptional age. Although the EEG patterns were comparable between the groups at the same age, analyses of the behavioral patterns of concordance in NREM sleep showed that newborns in Group I had a more immature behavior than newborns in Group II. Our results also suggest that extrauterine life of preterm babies does not seem to accelerate EEG maturation but may influence the acquisition of behavioral patterns during NREM sleep.     

Short-term effects of fluoxetine and trifluoromethylphenylpiperazine on electroencephalographic sleep in the rat

Fluoxetine and trifluoromethylphenylpiperazine (TFMPP) were studied for their short-term effects on electroencephalographic sleep in male rats. Following single injection, each drug produced a sizeable, dose-related suppression of rapid-eye-movement (REM) sleep that persisted for 4-5 h (fluoxetine, 0.625-5 mg/kg; TFMPP, 0.10-1.25 mg/kg). TFMPP also consistently increased non-REM (NREM) sleep during the second hour after drug injection, though this effect was not dose-related (it was seen at all doses tested). Fluoxetine produced small effects on NREM sleep that varied non-systematically with dose and time after drug injection. TFMPP, but not fluoxetine, also increased at all doses the number of delta waves per minute of NREM sleep in the second hour. A structural analog of TFMPP that is inactive at serotonin (5-HT) receptors [4-(m-trifluoromethylphenyl)piperadine; LY97117] was also tested, and found to be devoid of effects on NREM and REM sleep. Both fluoxetine (a 5-HT reuptake blocker) and TFMPP (a 5-HT agonist) enhance transmission across 5-HT synapses, though by different mechanisms. Because they have the common effect of suppressing REM sleep, and in a dose-related manner, the data support the notion that 5-HT neurons in the brain, when active, can suppress REM sleep.