Consciousness in waking and dreaming: the roles of neuronal oscillation and neuromodulation in determining similarities and differences

State-dependent aspects of consciousness are explored with particular attention to waking and dreaming. First, those phenomenological differences between waking and dreaming that have been established through subjective reports are reviewed. These differences are robustly expressed in most aspects of consciousness including perception, attention, memory, emotion, orientation, and thought. Next, the roles of high frequency neuronal oscillation and neuromodulation are explored in waking and rapid eye movement sleep, the stage of sleep with which the most intense dreaming is associated. The high frequency neuronal oscillations serve similar functions in the wake and rapid eye movement states sleep but neuromodulation is very different in the two states. The collective high frequency oscillatory activity gives coherence to spatially separate neurons but, because of the different neuromodulation, the binding of sensory input in the wake state is very different from the binding of internally perceived input during rapid eye movement sleep. An explanatory model is presented which states that neuromodulation, as well as input source and brain activation level differentiate states of the brain, while the self-organized collective neuronal oscillations unify consciousness via long range correlations.     

Role of adenosine in behavioral state modulation: a microdialysis study in the freely moving cat

There is considerable evidence to suggest that the activity of forebrain and mesopontine cholinergic neurons is intimately involved in electroencephalographic arousal. Furthermore, our previous in vitro investigation suggested that both cholinergic systems are under a powerful tonic inhibitory control by endogenous adenosine. We thus examined the in vivo effect, on electrographically defined behavioral states, of microdialysis perfusion of adenosine into the cholinergic zones of the substantia innominata of the basal forebrain and the laterodorsal tegmental nucleus of freely moving cats. Localized perfusion of adenosine into either the basal forebrain or the laterodorsal tegmental nucleus caused a marked alteration in sleep-wake architecture. Adenosine (300 microM) perfused into either the basal forebrain or laterodorsal tegmental nucleus produced a dramatic decrease in waking, to about 50% of the basal level. Perfusion into the basal forebrain resulted in a significant increase in rapid eye movement sleep, while slow wave sleep was unchanged. In contrast, adenosine perfusion into the laterodorsal tegmental nucleus produced an increase of both slow wave sleep and rapid eye movement sleep, the magnitude of which were proportional to the decrease in waking. Electroencephalographic power spectral analysis showed that adenosine perfusion into the basal forebrain increased the relative power in the delta frequency band, whereas higher frequency bands (theta, alpha, beta and gamma) showed a decrease. These data strongly support the hypothesis that adenosine might play a key role as an endogenous modulator of wakefulness and sleep. The decrease in wakefulness may be directly related to the inhibition of cholinergic neurons of the basal forebrain and the laterodorsal tegmentum. The increase in rapid eye movement sleep is a novel but robust effect whose origin, at present, is uncertain. The observation that local perfusion of adenosine into either the basal forebrain or the laterodorsal tegmental nucleus dramatically decreases wakefulness suggests that these areas might represent a major site of action of the xanthine stimulants (adenosine antagonists) found in coffee and tea.     

Cholinergic responsiveness of neurons in the ventroposterior thalamus of the anesthetized rat

Acetylcholine has been implicated as an important neurotransmitter in the mechanisms of thalamic activation. Cholinergic mechanisms are thought to directly underlie the high level of excitability observed in thalamic relay neurons during waking and rapid eye movement sleep. We sought to determine if the cholinergic responsiveness of neurons in the ventroposterior nuclei of the thalamus in rat is consistent with this view. Neurons in the chloral hydrate-anesthetized rat were studied with extracellular recording and microiontophoretic application of cholinergic agents. In most cases (63% of 63 cells), the ejection of the agonist, carbachol, had no observable effect on spontaneous activity. Facilitation (25%), inhibition (8%) and inhibition followed by facilitation (3%) were also observed. Carbachol ejections that by themselves were ineffective in altering spontaneous activity proved capable, in 93% of 28 cells, of antagonizing the uniformly facilitatory responses produced by glutamate ejection. The putative M1-selective, cholinergic agonist, McN-A-343, was also ineffective alone in altering spontaneous activity in the majority of cases (74% of 27 cells) and produced only inhibitory responses in the remaining seven neurons studied. Interacting applications of McN-A-343 and glutamate resulted, in all cases, in antagonism of glutamate facilitation (N = 12). The various responses to applied cholinergic agonists were all capable of being antagonized by muscarinic receptor-blocking agents. Both the high proportion of inhibitory responses and the antagonism of glutamate facilitatory responses suggest that ventroposterior neurons in the rat differ from other thalamocortical relay neurons in the rat and cat with regard to cholinergic responsiveness. Additionally, the lack of predominantly facilitatory responding renders it unlikely that cholinergic mechanisms directly underlie increases in excitability of ventroposterior neurons observed during waking and rapid eye movement sleep.     

Progressive cortical synchronization of ponto-geniculo-occipital potentials during rapid eye movement sleep

Phasic events, termed ponto-geniculo-occipital potentials, appear in the brainstem, thalamus and cerebral cortex during rapid eye movement sleep. In the cat, the species of choice for ponto-geniculo-occipital studies, these field potentials are usually recorded from the lateral geniculate thalamic nucleus and visual cortex. However, the fact that brainstem cholinergic neurons play a crucial role in the transfer of ponto-geniculo-occipital potentials to the thalamus, coupled with the evidence that mesopontine tegmental neurons project to virtually all thalamic nuclei, together explain why ponto-geniculo-occipital potentials are recorded over widespread territories, beyond the visual thalamocortical system. Here we demonstrate, by means of multi-site unit and field potential recordings from sensory, motor and association cortical areas in behaving cats, that: (i) ponto-geniculo-occipital potentials appear synchronously over the neocortex; and (ii) that their cortical synchronization develops progressively from the period preceding rapid eye movement sleep by 30-90 s (pre-rapid eye movement), to reach the highest degree of intracortical coherence during later epochs of rapid eye movement sleep. We propose that the widespread coherence of cortical ponto-geniculo-occipital potentials underlies the synchronization of fast oscillations (30-40 Hz) during rapid eye movement sleep over many, functionally distinct cortical territories implicated in dreaming, as brainstem-induced ponto-geniculo-occipital-like potentials are consistently followed by such fast oscillations.     

Frontal Electroencephalogram Alpha Asymmetry During Sleep: Stability and Its Relation to Affective Style.

Electroencephalogram (EEG) alpha (8-12 Hz) asymmetries were collected from the mid-frontal and central regions during presleep wakefulness and Stage 1, Stage 2, and rapid eye movement (REM) sleep in 11 healthy right-handed participants who were free of psychiatric, neurological, and sleep problems. The authors found significant correlations between presleep wakefulness and different stages of sleep in the frontal, but not central, EEG alpha asymmetry measure. The strongest correlation was between presleep waking and REM sleep, replicating and extending relation earlier work to a normal population. The high degree of association between presleep waking and REM sleep may be a result of high cortical activation common to these states and may reflect a predisposition to different styles of emotional reactivity. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Compensatory sleep responses to wakefulness induced by the dopamine autoreceptor antagonist (-)DS121

The effect of the dopamine autoreceptor antagonist (-)DS121 on wakefulness, locomotor activity, body temperature and subsequent compensatory sleep responses was examined in the rat. Animals entrained to a light-dark cycle were treated at 5 h after lights-on (CT-5) with 0.5, 1, 5 or 10 mg/kg i.p. (-)DS121 or methylcellulose vehicle. An additional group received 5 mg/kg i.p. (-)DS121 or vehicle 6 h after lights-off (CT-18). At CT-5, (-)DS121 dose-dependently increased wakefulness, locomotor activity and body temperature, and decreased both non-rapid eye movement sleep (NREM) and rapid eye movement sleep (REM) during the first 4 h post-treatment relative to vehicle controls. REM interference lasted up to 3 h longer than NREM. Low doses of (-)DS121 (0.5 and 1 mg/kg) produced relatively little waking that was not followed by significant compensatory sleep responses. In contrast, higher doses (5 and 10 mg/kg) produced compensatory hypersomnolence (robust increases in NREM immediately after the primary waking effect) that was proportional to the duration of drug-induced wakefulness. NREM recovery 24 h post-treatment was the same for the 5 mg/kg (65.4 +/- 9.9 min) and 10 mg/kg (64.8 +/- 9.3 min) doses, but was not proportional to prior wake duration. NREM displaced by drug-induced wakefulness was recovered completely by 24 h post-treatment at the 5 mg/kg dose, but only 63.5% recovered at 10 mg/kg. In contrast, equivalent wakefulness produced by sleep deprivation yielded 100% NREM recovery. At CT-18, (-)DS121 (5 mg/kg) increased wakefulness without disproportionately increasing locomotor activity, and was compensated fully by 24 h post-treatment. These data show that (-)DS121 dose-dependently increases wakefulness, which is followed by hypersomnolence that is proportional to drug-induced wake-promoting efficacy.     

Effects of accumbens m-chlorophenylbiguanide microinjections on sleep and waking in intact and 6-hydroxydopamine-treated rats

Effects of the 5-HT3 receptor agonist, m-chlorophenylbiguanide (10.0-40.0 microg), on sleep and waking were studied in control, vehicle-treated and 6-hydroxydopamine-injected rats. Bilateral injections of m-chlorophenylbiguanide into the nucleus accumbens of the control and the vehicle-infused animals significantly increased waking and reduced slow wave sleep. Rapid eye movement sleep (REM sleep) remained unchanged. Pretreatment with the selective 5-HT3 receptor antagonist, MDL 72222 (1aH,3a,5a, H-tropan-3-yl-3,5-dichloro-benzoate) (0.5 mg/kg, s.c.), reversed the effects of m-chlorophenylbiguanide (10.0-20.0 microg) on sleep and waking in the control group. Administration of the 5-HT3 receptor agonist to the 6-hydroxydopamine-treated animals modified only slightly the time spent in wakefulness and slow wave sleep, while REM sleep was significantly and dose dependently reduced. Our findings further support the proposal that increase of wakefulness and reduction of slow wave sleep after activation of 5-HT3 receptors, is partly related to the release of endogenous dopamine.     

In vitro release of acyclovir from semisolid dosage forms: effect of cyclodextrin and polyethylene glycol

Presynaptic depolarization of trigemino-thalamic (TGT) terminals may contribute to modulation of ascending oro-facial somatosensory information during active (or rapid eye movement) sleep. The relative excitability of TGT terminals was inferred from changes in the current required to maintain an antidromic firing probability of 50% (EC50) during quiet wakefulness as compared to active sleep. Depolarization or hyperpolarization of TGT terminals was defined as a decrease or increase, respectively, in the EC50. Overall, the EC50 of 8 TGT terminals was reduced by a mean 8.8+/-3.6 microA during active sleep relative to quiet wakefulness. This result suggests that depolarization of TGT terminals, which may act to suppress the transfer of sensory information from the trigeminal nucleus to the thalamus, occurs during active sleep.     

Spectral characteristics of sleep EEG in chronic insomnia

To determine whether the spectral characteristics of the sleep electroencephalogram (EEG) of insomniacs differ from that of healthy subjects, we compared in each of the first four non-rapid eye movement (NREM) and rapid eye movement (REM) episodes: (a) the time courses of absolute power, averaged over the subjects in each group, for the delta, theta, alpha, sigma and beta frequency bands; (b) the relationship between these time courses; and (c) the overnight trend of integrated power in each frequency band. The results show that NREM power, for all frequencies below the beta range, has slower rise rates and reaches lower levels in the insomniac group, whereas beta power is significantly increased. In REM, insomniacs show lower levels in the delta and theta bands, whereas power in the faster frequency bands is significantly increased. Thus, the pathophysiology of insomnia is characterized not only by the generally acknowledged slow wave deficiency, but also by an excessive hyperarousal of the central nervous system throughout the night, affecting both REM and NREM sleep. This hyperarousal is interpreted in terms of the neuronal group theory of sleep which provides a possible explanation for the discrepancies observed between subjective impressions and objective measures of sleep. Also, it is suggested that the progressive hyperpolarization of the thalamocortical neurons as sleep deepens is slower in the patient population and that this may explain the observed slow wave deficiency. The homeostatic control of slow wave activity, on the other hand, would appear to be intact in the patient population.     

Contrasting expressions of aggressive behavior released by lesions of the central nucleus of the amygdala during wakefulness and rapid eye movement sleep without atonia in cats.

Whether damage to the central nucleus of the amygdala (Ace) contributes to the predatory-like attack sometimes observed in rapid eye movement sleep without atonia (REM-A), created in cats by bilateral pontine lesions, was examined. Such lesions eliminate REM sleep skeletal muscle atonia and release elaborate behavior. Unilateral damage to the Ace alone increased affective defensive aggressive behavior toward humans and conspecifics without altering predatory behavior in wakefulness. Pontine lesions added at loci normally not leading to aggression induced predatory-like attacks in REM-A as well as the waking affective defense. Alterations of autonomic activity, the absence of relevant environmental stimuli in REM-A, or both may explain the state-related differences. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Behavioral state control through differential serotonergic inhibition in the mesopontine cholinergic nuclei: a simultaneous unit recording and microdialysis study

Cholinergic neurons of the mesopontine nuclei are strongly implicated in behavioral state regulation. One population of neurons in the cholinergic zone of the laterodorsal tegmentum and the pedunculopontine nuclei, referred to as rapid eye movement (REM)-on neurons, shows preferential discharge activity during REM sleep, and extensive data indicate a key role in production of this state. Another neuronal group present in the same cholinergic zone of the laterodorsal tegmentum and the pedunculopontine nuclei, referred to as Wake/REM-on neurons, shows preferential discharge activity during both wakefulness and REM sleep and is implicated in the production of electroencephalographic activation in both of these states. To test the hypothesis of differential serotonergic inhibition as an explanation of the different state-related discharge activity, we developed a novel methodology that enabled, in freely behaving animals, simultaneous unit recording and local perfusion of neuropharmacological agents using a microdialysis probe adjacent to the recording electrodes. Discharge activity of REM-on neurons was almost completely suppressed by local microdialysis perfusion of the selective 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), although this agonist had minimal or no effect on the Wake/REM-on neurons. We conclude that selective serotonergic inhibition is a basis of differential state regulation in the mesopontine cholinergic nuclei, and that the novel methodology combining neurophysiological and neuropharmacological information from the freely behaving animal shows great promise for further insight into the neural basis of behavioral control.     

Contributions of the pedunculopontine region to normal and altered REM sleep

The pedunculopontine (PPN) region of the upper brainstem is recognized as a critical modulator of activated behavioral states such as wakefulness and rapid eye movement (REM) sleep. The expression of REM sleep-related physiology (e.g. thalamocortical arousal, ponto-geniculate-occipital (PGO) waves, and atonia) depends upon a subpopulation of PPN neurons that release acetylcholine (ACh) to act upon muscarinic receptors (mAChRs). Serotonin's potent hyperpolarization of cholinergic PPN neurons is central to present working models of REM sleep control. A growing body of experimental evidence and clinical experience suggests that the responsiveness of the PPN region, and thereby modulation of REM sleep, involves closely adjacent glutamatergic neurons and alternate afferent neurotransmitters. Although many of these afferents are yet to be defined, dopamine-sensitive GABAergic pathways exiting the main output nuclei of the basal ganglia and adjacent forebrain nuclei appear to be the most conspicuous and the most likely to be clinically relevant. These GABAergic pathways are ideally sited to modulate the physiologic hallmarks of REM sleep differentially (e.g. atonia versus cortical activation), because each originates from a functionally unique forebrain circuit and terminates in a unique pattern upon brain stem neurons with unique membrane characteristics. Evidence is reviewed that changes in the quality, timing, and quantity of REM sleep that characterize narcolepsy, REM sleep behavior disorder, and neurodegenerative and affective disorders (depression and schizophrenia) reflect 1) changes in responsiveness of cells in the PPN region governed by these afferents; 2) increase or decrease in PPN cell number; or 3) mAChRs mediating increased responsiveness to ACh derived from the PPN. Auditory evoked potentials and acoustic startle responses provide means independent from recording sleep to assess pathophysiologies affecting the PPN and its connections and thereby complement investigations of their role in affecting daytime functions (e.g. arousal and attention).     

The correlation between changes in EEG and eye movement (EOG) accompanied by lowered arousal level

We investigated the correlation between the components of spontaneous eye movement (EOG) and EEG in six healthy individuals. The study was conducted in three periods; from the resting to drowsy stage, from the drowsy to spontaneous awakening stage, and in the forced waking stage. EEG, as registered from bipolar electrodes attached between the left parietal region (P3) and the left occipital region (O1), was monitored continuously by the FFT method with a segment of 12.8 seconds. Rapid eye movement and slow eye movement were observed simultaneously. In conclusion, even when the arousal level varies considerably, there is a close correlation between frequency of rapid eye movement and EEG patterns of 10.16 integral of 10.94 Hz & 17.97 integral of 19.53 Hz (simple correlation p < 0.01). Additionally, during the forced waking period (after stage 2), delta and theta bands increased in cases along with sleepiness. Even if the depth of sleep was the same, one's mood upon awakening was determined by the frequency of slow waves before awakening.     

Relationship between sleep patterns and human colonic motor patterns

BACKGROUND/AIMS: The precise relationships among colonic motor patterns, depth of sleep, and awakening are incompletely understood. The aim of this study was to correlate human colonic motor patterns with sleep stage, nocturnal arousals, and waking. METHODS: We monitored sleep and correlated sleep stage, arousals, and waking with pressures (area under curve and propagating contractions) recorded from the entire colon in 11 healthy volunteers. RESULTS: Propagating contraction frequency (P = 0.01) and area under the curve (P = 0.001) were significantly reduced at night. There was a highly significant correlation between depth of sleep and suppression of area under curve (P = 0.001) and propagating contraction frequency (P = 0.0001). Propagating contractions were eliminated during slow-wave sleep. During rapid eye movement sleep, colonic pressure and propagating contraction frequency increased sharply to levels comparable with those found in stage 2 sleep. Transient arousal from stable sleep, with or without waking, was a potent and immediate stimulus for colonic propagating contractions. CONCLUSIONS: Sleep per se has a profound inhibitory effect on propagating and nonpropagating activity and is the major determinant of diurnal variation of colonic motility. Propagating contractions are eliminated in slow-wave sleep. Rapid eye movement sleep, arousals, and waking have immediate stimulatory effects on colonic motility.     

Respiratory and body movements as indicators of sleep stage and wakefulness in infants and young children

Conventional polysomnographic (PSG) sleep staging to sleep staging based on a static-charge-sensitive bed (SCSB) recording in infants and young children was compared. The study consisted of whole-night clinical sleep studies in 22 children at 24 weeks (SD 24, range 1-79 weeks) of age. Most of the children presented with respiratory disturbances during sleep. From the SCSB record, sleep stages were differentiated according to regularity of breathing, presence of body movements, and most important, presence of high-frequency components of breathing (SCSB spikes). With both methods, three sleep/wake stages were distinguished: rapid eye movement (REM) sleep, non-rapid eye movement (NREM) sleep and wakefulness. The average interscorer reliability of the PSG sleep staging controlled in nine subjects was 88%. The average concordance between the two methods ranged from 82 to 85%, depending on the criteria used for scoring the SCSB. The mean sensitivity of the SCSB to detect NREM sleep ranged from 77 to 90% and the mean sensitivity to detect REM sleep ranged from 61 to 86%. The mean positive predictive value was 89-96% for NREM sleep and 54-67% for REM sleep. In conclusion, REM sleep is characterized by irregular breathing with superimposed fast respiratory movements. These changes are specific enough to allow distinction between episodes of NREM sleep, REM sleep and wakefulness with the non-invasive SCSB method in infants and young children. Incomplete concordance between PSG and SCSB score was most frequently observed during sleep stage transition periods, where the behavioural state and electrophysiological criteria disagreed. When combined with the PSG, the SCSB provides complementary information about the behavioural state of child.     

Respiratory responses to tracheobronchial stimulation during sleep and wakefulness in the adult cat

The response to tracheal stimulation (50 microliters of tap water) during wakefulness, non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep was investigated in adult cats. In wakefulness, repetitive coughing occurred on 80% of the trials. In NREM and REM sleep, the most frequent response (approximately 69% and 58% of the trials, respectively) was arousal, followed by coughing. Apneas occurred following the stimulus and before arousal in 11% and 24% of the trials in NREM and REM sleep, respectively. In NREM sleep, the tracheal stimulus sometimes evoked expiratory efforts following a normal inspiratory effort (11% of the trials). These were much weaker than the expiratory efforts during coughing in wakefulness. In REM sleep, stimulation in 11% of the trials elicited increased inspiratory efforts. Although these may have been diminutive preparatory inspirations for coughing, they were much smaller than preparatory inspirations associated with coughing in wakefulness, and they were never followed by active expiratory efforts. Arousal from either NREM or REM sleep in response to tracheal stimulation was sometimes associated with an augmented breath. This response, which is common upon spontaneous arousal, may lead to deeper aspiration of the tracheal fluid. We conclude that in cats coughing requires wakefulness and that airway stimuli in sleep cause a variety of respiratory responses, some of which may be maladaptive.     

Changes in EEG power density during sleep laboratory adaptation

First- and second-night effects on the electroencephalogram (EEG) were investigated by means of polygraphic sleep recordings and all-night spectral analysis. Eighteen normal subjects were studied for three consecutive nights in a hospital sleep laboratory. Visual sleep scoring showed that there was a first-night effect in normal subjects similar to that reported previously [increased wakefulness; decreased total sleep time, sleep efficiency, and rapid eye movement (REM) sleep]. Spectral analysis of the sleep EEG revealed important changes, most of which occurred in REM sleep. Increased delta, theta, and beta1 power densities accompanied by decreased mean frequency were seen in REM sleep in the second night. On the basis of REM sleep deprivation results previously published, our data suggest that the second night could be affected by partial REM sleep deprivation that occurred in the first night. Delta and theta power density values decreased in the first non-rapid eye movement episode of nights 1 and 2; this could result from increased REM sleep pressure. The overall consistency of spectral data in the first and second night with REM sleep findings derived from visual scoring in the first night lends further support to this hypothesis. The sleep disturbance experienced during the first night in a sleep laboratory may be a useful and valid model of transient insomnia. Therefore, we conclude that data from all nights recorded should be included in assessing a subject's sleep.     

Coherence analysis of the human sleep electroencephalogram

Animal studies have shown that the sleep-related oscillations in the frequency range of spindles and slow-waves, and in the gamma band occur synchronously over large parts of the cerebral cortex. Coherence analysis was used to investigate these oscillations in the human sleep electroencephalogram. In all-night electroencephalogram recordings from eight young subjects power and coherence spectra within and between cerebral hemispheres were computed from bipolar derivations placed bilaterally along the antero-posterior axis. The 0.75-50 Hz range was examined with a resolution of 0.25 Hz. Distinct peaks in coherence were present in non-rapid eye movement sleep but not in rapid eye movement sleep. The most prominent and consistent peak was seen in the range of sleep spindles (13-14 Hz), and additional peaks were present in the alpha band (9-10 Hz) and low delta band (1-2 Hz). Whereas coherence in the spindle range was highest in stage 2, the alpha peak was most prominent in slow-wave sleep (stages 3 and 4). Interhemispheric coherence at 30 Hz was higher in rapid eye movement sleep than in non-rapid eye movement sleep. There were also marked sleep state-independent regional differences. Coherence between homologous interhemispheric derivations was high in the low frequency range and declined with increasing frequencies, whereas coherence of intrahemispheric and non-homologous interhemispheric derivations was at a low level throughout the spectra. It is concluded that coherence analysis may provide insights into large-scale functional connectivities of brain regions during sleep. The high coherence of sleep spindles is an indication for their widespread and quasi-synchronous occurrence throughout the cortex and may point to their specific role in the sleep process.     

Monotremes and the evolution of rapid eye movement sleep

Early studies of the echidna led to the conclusion that this monotreme did not have rapid eye movement (REM) sleep. Because the monotremes had diverged from the placental and marsupial lines very early in mammalian evolution, this finding was used to support the hypothesis that REM sleep evolved after the start of the mammalian line. The current paper summarizes our recent work on sleep in the echidna and platypus and leads to a very different interpretation. By using neuronal recording from mesopontine regions in the echidna, we found that despite the presence of a high-voltage cortical electroencephalogram (EEG), brainstem units fire in irregular bursts intermediate in intensity between the regular non-REM sleep pattern and the highly irregular REM sleep pattern seen in placentals. Thus the echidna displays brainstem activation during sleep with high-voltage cortical EEG. This work encouraged us to do the first study of sleep, to our knowledge, in the platypus. In the platypus we saw sleep with vigorous rapid eye, bill and head twitching, identical in behaviour to that which defines REM sleep in placental mammals. Recording of the EEG in the platypus during natural sleep and waking states revealed that it had moderate and high-voltage cortical EEGs during this REM sleep state. The platypus not only has REM sleep, but it had more of it than any other animal. The lack of EEG voltage reduction during REM sleep in the platypus, and during the REM sleep-like state of the echidna, has some similarity to the sleep seen in neonatal sleep in placentals. The very high amounts of REM sleep seen in the platypus also fit with the increased REM sleep duration seen in altricial mammals. Our findings suggest that REM sleep originated earlier in mammalian evolution than had previously been thought and is consistent with the hypothesis that REM sleep, or a precursor state with aspects of REM sleep, may have had its origin in reptilian species.     

The mismatch negativity to frequency deviants during the transition from wakefulness to sleep.

Examined the changes in the mismatch negativity (MMN) during the transition from a waking, conscious state to one of sleep and unconsciousness. Auditory event-related potentials were recorded from 8 Ss, 21–32-yrs old, during the sleep onset period. A 1,000 Hz-standard stimulus was presented every 600 ms. At random, on 20% of the trials, the standard was changed to either a large 2,000-Hz or a small 1,100-Hz deviant. Results indicate that during wakefulness, the large deviant elicited a larger, long-lasting MMN than the small deviant. Following the large deviant during relaxed wakefulness and Stage 2 sleep, the MMN continued to be elicited although it was reduced in amplitude. No significant MMN was recorded for either deviant in Stages 1 and slow wave sleep. The loss of consciousness therefore appears to have a marked effect on the MMN. (PsycINFO Database Record (c) 2010 APA, all rights reserved)