Showing papers on "Rapid eye movement sleep published in 2000"
TL;DR: A three-dimensional model with specific examples from normally and abnormally changing conscious states of REM sleep dreaming is presented, suggesting that there are isomorphisms between the phenomenology and the physiology of dreams.
Abstract: Sleep researchers in different disciplines disagree about how fully dreaming can be explained in terms of brain physiology. Debate has focused on whether REM sleep dreaming is qualitatively different from nonREM (NREM) sleep and waking. A review of psychophysiological studies shows clear quantitative differences between REM and NREM mentation and between REM and waking mentation. Recent neuroimaging and neurophysiological studies also differentiate REM, NREM, and waking in features with phenomenological implications. Both evidence and theory suggest that there are isomorphisms between the phenomenology and the physiology of dreams. We present a three-dimensional model with specific examples from normally and abnormally changing conscious states.
917 citations
TL;DR: The results suggest that, in the case of this visual discrimination task, both SWS and REM are required to consolidate experience-dependent neuronal changes into a form that supports improved task performance.
Abstract: Performance on a visual discrimination task shows long-term improvement after a single training session. When tested within 24 hr of training, improvement was not observed unless subjects obtained at least 6 hr of post-training sleep prior to retesting, in which case improvement was proportional to the amount of sleep in excess of 6 hr. For subjects averaging 8 hr of sleep, overnight improvement was proportional to the amount of slow wave sleep (SWS) in the first quarter of the night, as well as the amount of rapid eye movement sleep (REM) in the last quarter. REM during the intervening 4 hr did not appear to contribute to improvement. A two-step process, modeling throughput as the product of the amount of early SWS and late REM, accounts for 80 percent of intersubject variance. These results suggest that, in the case of this visual discrimination task, both SWS and REM are required to consolidate experience-dependent neuronal changes into a form that supports improved task performance.
541 citations
TL;DR: These findings suggest that the fore brain mechanism in question is the final common path to dreaming and that the brainstem oscillator that controls the REM state is just one of the many arousal triggers that can activate this forebrain mechanism.
Abstract: The paradigmatic assumption that REM sleep is the physiological equivalent of dreaming is in need of fundamental revision. A mounting body of evidence suggests that dreaming and REM sleep are dissociable states, and that dreaming is controlled by forebrain mechanisms. Recent neuropsychological, radiological, and pharmacological findings suggest that the cholinergic brain stem mechanisms that control the REM state can only generate the psychological phenomena of dreaming through the mediation of a second, probably dopaminergic, forebrain mechanism. The latter mechanism (and thus dreaming itself) can also be activated by a variety of nonREM triggers. Dreaming can be manipulated by dopamine agonists and antagonists with no concomitant change in REM frequency, duration, and density. Dreaming can also be induced by focal forebrain stimulation and by complex partial (forebrain) seizures during nonREM sleep, when the involvement of brainstem REM mechanisms is precluded. Likewise, dreaming is obliterated by focal lesions along a specific (probably dopaminergic) forebrain pathway, and these lesions do not have any appreciable effects on REM frequency, duration, and density. These findings suggest that the forebrain mechanism in question is the final common path to dreaming and that the brainstem oscillator that controls the REM state is just one of the many arousal triggers that can activate this forebrain mechanism. The "REM-on" mechanism (like its various NREM equivalents) therefore stands outside the dream process itself, which is mediated by an independent, forebrain "dream-on" mechanism.
527 citations
TL;DR: It is proposed that hcrt receptor 1 in the LC is a key target for REM sleep regulation and might be involved in the pathophysiological mechanisms of narcolepsy.
Abstract: The hypocretins (hcrts), also known as orexins, are two recently identified excitatory neuropeptides that in rat are produced by ∼1200 neurons whose cell bodies are located in the lateral hypothalamus. The hypocretins/orexins have been implicated in the regulation of rapid eye movement (REM) sleep and the pathophysiology of narcolepsy. In the present study, we investigated whether the locus coeruleus (LC), a structure receiving dense hcrtergic innervation, which is quiescent during REM sleep, might be a target for hcrt to regulate REM sleep. Local administration of hcrt1 but not hcrt2 in the LC suppressed REM sleep in a dose-dependent manner and increased wakefulness at the expense of deep, slow-wave sleep. These effects were blocked with an antibody that neutralizes hcrt binding to hcrt receptor 1. In situ hybridization and immunocytochemistry showed the presence of hcrt receptor 1 but not the presence of hcrt receptor 2 in the LC. Iontophoretic application of hcrt1 enhanced the firing rate of LC neurons in vivo, and local injection of hcrt1 into the LC induced the expression of c-fos in the LC area. We propose that hcrt receptor 1 in the LC is a key target for REM sleep regulation and might be involved in the pathophysiological mechanisms of narcolepsy.
489 citations
TL;DR: The unique pattern of sleep-related changes in basal forebrain adenosine level lends strong support to the hypothesis that the sleep-promoting effects of adenosines, as well as the sleepiness associated with prolonged wakefulness, are both mediated by adenosinergic inhibition of a cortically projecting basal fore brain arousal system.
428 citations
TL;DR: In a preliminary attempt to reconcile the two models, an alternative model is proposed that assumes the existence of covert REM sleep processes during NREM sleep, which may be responsible for much of the dreamlike cognitive activity occurring in NREMSleep.
Abstract: Numerous studies have replicated the finding of mentation in both rapid eye movement (REM) and nonrapid eye movement (NREM) sleep. However, two different theoretical models have been proposed to account for this finding: (1) a one-generator model, in which mentation is generated by a single set of processes regardless of physiological differences between REM and NREM sleep; and (2) a two-generator model, in which qualitatively different generators produce cognitive activity in the two states. First, research is reviewed demonstrating conclusively that mentation can occur in NREM sleep; global estimates show an average mentation recall rate of about 50% from NREM sleep--a value that has increased substantially over the years. Second, nine different types of research on REM and NREM cognitive activity are examined for evidence supporting or refuting the two models. The evidence largely, but not completely, favors the two-generator model. Finally, in a preliminary attempt to reconcile the two models, an alternative model is proposed that assumes the existence of covert REM sleep processes during NREM sleep. Such covert activity may be responsible for much of the dreamlike cognitive activity occurring in NREM sleep.
414 citations
TL;DR: Sleep stage analyses indicated that the nocturnal increase in IL-6 occurred in association with stage 1-2 sleep and rapid eye movement sleep, but levels during slow wave sleep were not different from those while awake.
Abstract: The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on circulating concentrations of interleukin-6 (IL-6) in relation to the secretory profiles of GH, cortisol, and melatonin. In 31 healthy male volunteers, blood samples were obtained every 30 min during 2 nights: uninterrupted, baseline sleep and partial sleep deprivation-early night (awake until 0300 h). Sleep was measured by electroencephalogram polysomnography. Sleep onset was associated with an increase in serum levels of IL-6 (P < 0.05) during baseline sleep. During PSD-E, the nocturnal increase in IL-6 was delayed until sleep at 0300 h. Sleep stage analyses indicated that the nocturnal increase in IL-6 occurred in association with stage 1-2 sleep and rapid eye movement sleep, but levels during slow wave sleep were not different from those while awake. The profile of GH across the 2 nights was similar to that of IL-6, whereas the circadian-driven hormones cortisol and melatonin showed no concordance with sleep. Loss of sleep may serve to decrease nocturnal IL-6 levels, with effects on the integrity of immune system functioning. Alternatively, given the association between sleep stages and IL-6 levels, depressed or aged populations who show increased amounts of REM sleep and a relative loss of slow wave sleep may have elevated nocturnal concentrations of IL-6 with implications for inflammatory disease risk.
392 citations
TL;DR: The firing of multiple single neurons in the hippocampus, a structure that is important for episodic memory, during familiar and novel experiences and in subsequent REM sleep is studied, showing a reversal of firing phase relative to local theta oscillations in REM sleep.
297 citations
TL;DR: REM sleep behavior disorder (RBD) is a possible herald of neurodegenerative disorders with parkinsonism, and the density of striatal dopaminergic terminals with [11C]dihydrotetrabenazine PET in subjects with RBD is determined.
Abstract: Article abstract—REM sleep behavior disorder (RBD) is a possible herald of neurodegenerative disorders with parkinsonism. The authors determined the density of striatal dopaminergic terminals with [ 11 C]dihydrotetrabenazine PET in six elderly subjects with chronic idiopathic RBD and 19 age-appropriate controls. In subjects with RBD, there were significant reductions in striatal [ 11 C]dihydrotetrabenazine binding, particularly in the posterior putamen.
277 citations
Journal Article•
TL;DR: The results have implications for analyzing diurnal variation of mood in unipolar and bipolar affective disorders and sleep disturbances in other major psychiatric conditions such as chronic schizophrenia.
Abstract: Recent evidence shows that the temporal alignment between the sleep-wake cycle and the circadian pacemaker affects self-assessment of mood in healthy subjects. Despite the differences in affective state between healthy subjects and patients with psychiatric disorders, these results have implications for analyzing diurnal variation of mood in unipolar and bipolar affective disorders and sleep disturbances in other major psychiatric conditions such as chronic schizophrenia. In a good proportion of patients with depression, mood often improves over the course of the day; an extension of waking often has an antidepressant effect. Sleep deprivation has been described as a treatment for depression for more than 30 years, and approximately 50% to 60% of patients with depression respond to this approach, especially those patients who report that their mood improves over the course of the day. The mechanisms by which sleep deprivation exerts its antidepressant effects are still controversial, but a reduction in rapid eye movement sleep (REM sleep), sleep pressure and slow-wave sleep (SWS), or a circadian phase disturbance, have been proposed. Although several studies support each of these hypotheses, none is sufficient to explain all observations reported to date. Unfortunately, the disturbed sleep-wake cycle or behavioural activities of depressed patients often explain several of the abnormalities reported in the diurnal rhythms of these patients. Thus, protocols that specifically manipulate the sleep-wake cycle to unmask the expression of the endogenous circadian pacemaker are greatly needed. In chronic schizophrenia, significant disturbances in sleep continuity, REM sleep, and SWS have been consistently reported. These disturbances are different from those observed in depression, especially with regard to REM sleep. Circadian phase abnormalities in schizophrenic patients have also been reported. Future research is expected to clarify the nature of these abnormalities.
259 citations
TL;DR: It is believed that the cumulative evidence indicates that REM sleep serves no role in the processing or consolidation of memory, and is proposed that the primary function of REM sleep is to provide periodic endogenous stimulation to the brain which serves to maintain requisite levels of central nervous system activity throughout sleep.
Abstract: We present evidence disputing the hypothesis that memories are processed or consolidated in REM sleep. A review of REM deprivation (REMD) studies in animals shows these reports to be about equally divided in showing that REMD does, or does not, disrupt learning/memory. The studies supporting a relationship between REM sleep and memory have been strongly criticized for the confounding effects of very stressful REM deprivation techniques. The three major classes of antidepressant drugs, monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), and selective serotonin reuptake inhibitors (SSRIs), profoundly suppress REM sleep. The MAOIs virtually abolish REM sleep, and the TCAs and SSRIs have been shown to produce immediate (40-85%) and sustained (30-50%) reductions in REM sleep. Despite marked suppression of REM sleep, these classes of antidepressants on the whole do not disrupt learning/memory. There have been a few reports of patients who have survived bilateral lesions of the pons with few lingering complications. Although these lesions essentially abolished REM sleep, the patients reportedly led normal lives. Recent functional imaging studies in humans have revealed patterns of brain activity in REM sleep that are consistent with dream processes but not with memory consolidation. We propose that the primary function of REM sleep is to provide periodic endogenous stimulation to the brain which serves to maintain requisite levels of central nervous system (CNS) activity throughout sleep. REM is the mechanism used by the brain to promote recovery from sleep. We believe that the cumulative evidence indicates that REM sleep serves no role in the processing or consolidation of memory.
TL;DR: Temporal lobe complex partial seizures decrease REM sleep, particularly when occurring during sleep but also when occurring on the previous day, which may be responsible for the prolonged impairment of functioning that some patients report following seizures.
Abstract: Background: Patients with brief, complex partial seizures frequently suffer from tiredness and decreased productivity that continue well beyond the postictal period. A possible explanation is that seizures, even when occurring during the day, disrupt sleep the following night. Objective: To determine the effect of temporal lobe complex partial seizures on sleep structure and daytime drowsiness. Methods: Patients with temporal lobe epilepsy were admitted for video-electroencephalography monitoring. Allnight polysomnography was recorded under the following 3 conditions: seizure free, seizure during the day before the recording, and seizure during the recording. Percentage of time in each sleep stage, sleep efficiency, and time to first and second rapid eye movement (REM) period were compared for seizure vs control conditions. Daytime drowsiness was also measured, using a modified maintenance of wakefulness test and 2 subjective drowsiness tests. Results: Daytime seizures reduced REM from 18% ± 1% to 12% ± 2% (P = .003). Night seizures reduced REM from 16% ±1 % to 6.8% ±2 % ( P ,.001). Night seizures also significantly reduced stages 2 and 4 while increasing stage 1 sleep. Night seizures, but not day seizures, significantly reduced sleep efficiency, increased time to first REM period, and increased drowsiness as measured by the maintenance of wakefulness test. Conclusions: Temporal lobe complex partial seizures decrease REM sleep, particularly when occurring during sleep but also when occurring on the previous day. This may, in part, be responsible for the prolonged impairment of functioning that some patients report following seizures. Arch Neurol. 2000;57:363-368
TL;DR: The results suggest the existence of a sleep pattern in autistic patients different from that observed in subjects with mental retardation and from that of normal controls, and indicate that sleep parameters in these patients are correlated with some psychological indices generally used for the diagnosis of autistic disorder.
Abstract: Polysomnography (EOG, EEG, EMG) was carried out in 17 male children and adolescents with autistic disorder, in seven patients with mental retardation and fragile X syndrome, and in five age- and sex-matched normal male subjects. Density of rapid eye movements was not significantly different in the three groups of subjects; however, some sleep parameters such as time in bed, sleep period time, and total sleep time were significantly lower in subjects with autistic disorder than in normal controls; moreover, patients with autistic disorder showed values of sleep period time, first REM latency and percent (%) sleep stage 1 lower than those of patients with fragile X syndrome with mental retardation. Density of muscle twitches was significantly higher in patients with autistic disorder than in normal controls. In contrast only minor differences were observed between patients with autistic disorder and those with fragile X syndrome with mental retardation. Furthermore, some psychoeducational profile-revised items such as perception and eye-hand coordination, showed significant correlation with some sleep parameters (time in bed, sleep latency, stage shifts, first REM latency and wakefulness after sleep onset). Childhood Autism Rating Scale (CARS) scores to visual response and non-verbal communication showed significant correlation with some tonic sleep parameters, such as sleep period time, wakefulness after sleep onset, and total sleep time. Relating to people and activity level items were found to be significantly correlated with rapid eye movement density. Our results suggest the existence of a sleep pattern in autistic patients different from that observed in subjects with mental retardation and from that of normal controls. In addition, these findings indicate that sleep parameters in these patients are correlated with some psychological indices generally used for the diagnosis of autistic disorder; for this reason, polysomnographies might be useful in the comprehension of the neurophysiological mechanisms underlying this condition.
TL;DR: Three patients with REM behavior disorder whose nocturnal symptoms were markedly improved by treatment with the acetylcholinesterase inhibitor donepezil are reported.
Abstract: Three patients with REM behavior disorder whose nocturnal symptoms were markedly improved by treatment with the acetylcholinesterase inhibitor donepezil are reported. Donepezil may have a role in the treatment of REM behavior disorder, possibly through its actions on cholinergic pathways in the brainstem.
TL;DR: A 75-year-old woman admitted to a hospital complaining of frequent episodes of transient dizziness and abnormal nocturnal behavior is reported with a patient with RBD with the sole lesion in the pontine reticular formation that could cause the abnormality of REM-mediated muscle atonia.
Abstract: REM sleep behavior disorder (RBD) is characterized by lack of atonia of major muscle groups during REM sleep associated with excessive movement related to dreaming.1 Various neurodegenerative diseases involving brainstem structures have been reported to be associated with RBD.2 We report a patient with RBD with the sole lesion in the pontine reticular formation that could cause the abnormality of REM-mediated muscle atonia.
A 75-year-old woman was admitted to our hospital complaining of frequent episodes of transient dizziness and abnormal nocturnal behavior. This behavior started about 10 years before, when she also had a TIA manifesting as transient weakness in the right upper and lower extremities. She had a 9-year history of diabetes mellitus and hypertension, both of which were well controlled on diet and exercise therapy. Her nocturnal behavior was characterized by waving her arms, beating herself at the wall, and kicking the bedclothes. During these episodes, she often shouted because she became angry with employees of her company in her …
TL;DR: Mirtazapine significantly improves sleep continuity in major depressive disorder patients with poor sleep quality at weeks 1 and 2 of treatment, while preserving sleep architecture.
TL;DR: The hypothesis that sleep organization, i.e. the regular occurrence of NREM-REM cycles more than sleep states per se, may be crucial for the retention of verbal material presented before sleep is put forward.
TL;DR: Alterations in REM and arousals characterized PTSD in this sample of elderly males exposed to war trauma 28-50 years ago, and when comorbid sleep disorders were ruled out, sleep was clinically similar across the groups.
TL;DR: REM sleep and mood state were related to low progesterone levels during the menstrual cycle, but postpartum REM sleep and Mood state wererelated to increased wake time rather than changes in progester one levels.
Abstract: Study objectives To test the hypotheses that: 1) an increase in endogenous progesterone levels during the luteal phase of the menstrual cycle will alter REM sleep and mood state, and 2) a decrease in endogenous progesterone levels during postpartum will also alter REM sleep and mood state. Design A longitudinal descriptive study utilizing ambulatory polysomnography for two consecutive nights at seven time points. Setting Subject's homes. Participants The first hypothesis was tested with 34 women studied during both the follicular and luteal phases of their menstrual cycle. The second hypothesis was tested with 31 women who completed the sleep studies during pregnancy and at one month postpartum. Interventions N/A. Measurements and results Women who ovulated (high levels of serum progesterone in the luteal phase) had shorter REM latency, more REM sleep, and more positive mood state compared to those who did not ovulate (low luteal progesterone). Compared to the third trimester (high progesterone), REM latency was significantly shorter at one month postpartum (low progesterone). Mood state was most positive at the second trimester and most negative at one month postpartum. Conclusions REM sleep and mood state were related to low progesterone levels during the menstrual cycle, but postpartum REM sleep and mood state were related to increased wake time rather than changes in progesterone levels.
TL;DR: Since the WKY rat represents a genetic model for depression with altered EEG sleep patterns, this strain may be particularly useful for investigating the relationship between depression and sleep abnormalities.
Abstract: The Wistar-Kyoto (WKY) rat exhibits several behavioral and hormonal abnormalities often associated with depression. One of the hallmarks of depression consists of alterations in the sleep-wake cycle, particularly in rapid eye movement (REM) sleep. If the WKY rat is indeed an animal model for depression, we hypothesized that it should also show sleep abnormalities relative to the control strain, the Wistar (WIS) rat Under baseline conditions, WKY rats showed a 50% increase in total REM sleep time during the 12 h light phase and an increase in sleep fragmentation during both the light and dark phase. The WKY rats also exhibited lower EEG power densities over the entire frequency range (0.2-25.0 Hz) during REM sleep. After a 6 h sleep deprivation, the REM sleep rebound was more pronounced during the dark but not the light phase in the WKY rats. Since the WKY rat represents a genetic model for depression with altered EEG sleep patterns, this strain may be particularly useful for investigating the relationship between depression and sleep abnormalities.
TL;DR: The findings show that 6 h RSD affected the NGF and BDNF protein levels in different manner, in the cerebellum and brainstem, and in the hippocampus, NGF was significantly decreased while BDNF was not changed.
TL;DR: Three old, overlapping theories of REM sleep (REM) function, the Ontogenetic, Homeostatic and Phylogenetic hypotheses, together still provide a plausible framework - that REM is directed towards early cortical development, "tones up" the sleeping cortex, can substitute for wakefulness, and has a calming effect.
TL;DR: Lesion analysis revealed that the candidate structures for PS erectile control include both the lateral preoptic area (LPOA) and ventral division of the bed nucleus of the stria terminalis; however, lesions of the LPOA were the most effective in disruptingPS erectile activity.
Abstract: Penile erections are a characteristic phenomenon of paradoxical sleep (PS), or rapid eye movement sleep. Although the neural mechanisms of PS-related erections are unknown, the forebrain likely plays a critical role (Schmidt et al., 1999). The preoptic area is implicated in both sleep generation and copulatory mechanisms, suggesting it may be a primary candidate in PS erectile control. Continuous recordings of penile erections, body temperature, and sleep-wake states were performed before and up to 3 weeks after ibotenic acid lesions of the preoptic forebrain in three groups of rats. Neurotoxic lesions involving the medial preoptic area (MPOA) and anterior hypothalamus (n = 5) had no significant effects on either erectile activity or sleep-wake architecture. In contrast, bilateral lesions of the lateral preoptic region, with (n = 4) or without (n = 5) MPOA involvement, resulted in a significant decrease in the number of erections per hour of PS, number of PS-related erections, and PS phases exhibiting an erection. Lesion analysis revealed that the candidate structures for PS erectile control include both the lateral preoptic area (LPOA) and ventral division of the bed nucleus of the stria terminalis; however, lesions of the LPOA were the most effective in disrupting PS erectile activity. LPOA lesioning also resulted in a long-lasting insomnia, characterized by the significant increase in wakefulness and decrease in slow wave sleep (SWS). PS architecture and waking-state erections remained unchanged after lesion in all groups. These data identify an essential role of the LPOA in both PS-related erectile mechanisms and SWS generation. Moreover, higher erectile mechanisms appear to be context-specific because LPOA lesioning selectively disrupted PS-related erections while leaving waking-state erections intact.
TL;DR: It is concluded that among patients suspected or confirmed to have OSA, one or more of these four variables-male sex, sleepiness, nocturnal REM sleep latency, and extent of oxygen desaturation-could reflect neurophysiological mechanisms responsible for 2omSOREMPs.
Abstract: Although 2 or more sleep onset rapid eye movement (REM) periods (2omSOREMPs) on a Multiple Sleep Latency Test (MSLT) raise the possibility of narcolepsy, patients with obstructive sleep apnea (OSA) also can have 2omSOREMPs, which may then cause diagnostic uncertainty. To explore what features among OSA patients predict 2omSOREMPs on an MSLT that follows nocturnal polysomnography, we reviewed data from 1,145 consecutively studied patients suspected or confirmed to have OSA rather than narcolepsy. Overall, 4.7% of the subjects had 2omSOREMPs. Variables that were independently predictive of 2omSOREMPs in logistic regression models included male gender (OR = 4.4, 95% CI = 1.9 to 12.7), a 5-min decrease in the MSLT-derived mean sleep latency (OR = 1.9, 95% CI = 1.3 to 2.8), a 90-min decrease in nocturnal latency to REM sleep (OR = 1.6, 95% CI = 1.1 to 2.5), and a 15-unit decrease in minimal recorded oxygen saturation (OR = 1.6, 95% CI = 1.3 to 2.0). We conclude that among patients suspected or confirmed to hav...
TL;DR: Examination of brain revealed Lewy bodies as well as marked neuronal loss in brainstem monoaminergic nuclei-particularly locus coeruleus and substantia nigra-that inhibit cholinergic neurons in the pedunculopontine nucleus mediating atonia during REM sleep.
Abstract: A patient with REM sleep behavior disorder who subsequently developed probable Lewy body dementia is now reported to have a definite pathologic diagnosis of Lewy body dementia. Examination of brain revealed Lewy bodies as well as marked neuronal loss in brainstem monoaminergic nuclei-particularly locus coeruleus and substantia nigra-that inhibit cholinergic neurons in the pedunculopontine nucleus mediating atonia during REM sleep.
TL;DR: The findings indicate that old rats, similar to elderly humans, demonstrate less sleep after prolonged wakefulness, and that although old rats have a decline in sleep, this cannot be attributed to loss of VLPO neurons implicated in sleep.
Abstract: There is a pronounced decline in sleep with age. Diminished output from the circadian oscillator, the suprachiasmatic nucleus, might play a role, because there is a decrease in the amplitude of the day-night sleep rhythm in the elderly. However, sleep is also regulated by homeostatic mechanisms that build sleep drive during wakefulness, and a decline in these mechanisms could also decrease sleep. Because this question has never been addressed in old animals, the present study examined the effects of 12 h wakefulness on compensatory sleep response in young (3.5 mo) and old (21.5 mo) Sprague-Dawley and F344 rats. Old rats in both strains had a diminished compensatory increase in slow-wave sleep (SWS) after 12 h of wakefulness (0700-1900, light-on period) compared with the young rats. In contrast, compensatory REM sleep rebound was unaffected by age. To assess whether the reduced SWS rebound in old rats might result from loss of neurons implicated in sleep generation, we counted the number of c-Fos immunoreactive (c-Fos-ir) cells in the ventral lateral preoptic (VLPO) area and found no differences between young and old rats. These findings indicate that old rats, similar to elderly humans, demonstrate less sleep after prolonged wakefulness. The findings also indicate that although old rats have a decline in sleep, this cannot be attributed to loss of VLPO neurons implicated in sleep.
TL;DR: IBS patients have greater sympathetic activity during waking and greater overall sympathetic dominance during rapid eye movement sleep, which support the presence of autonomic abnormalities in patients with IBS.
TL;DR: The cause of sleep is a complex question, which needs a clear distinction amongst the different meanings of a causal relationship in the study of a given behavior, the requisites to be met by a suggested cause, and a precise definition of sleep to distinguish behavioral from polygraphic sleep.
TL;DR: Evidence indicates the existence of a consistent relationship between slow-wave (SW) sleep and increased GH secretion, and compounds that increase SW sleep may therefore represent a novel class of GH secretagogues.
Abstract: In healthy young adults, the 24-hour profile of plasma growth hormone (GH) levels consists of stable low levels abruptly interrupted by bursts of secretion. In normal women, daytime GH secretory pulses are frequent. However, in normal men, a sleep-onset-associated pulse is generally the major or even the only daily episode of active secretion. Extensive evidence indicates the existence of a consistent relationship between slow-wave (SW) sleep and increased GH secretion. There is a linear relationship between the amount of SW sleep (measured by either visual scoring or spectral analysis of the EEG) and the amount of concomitant GH secretion. During ageing, SW sleep and GH secretion decrease exponentially and with the same chronology. Pharmacological stimulation of SW sleep results in increased GH release, and compounds that increase SW sleep may therefore represent a novel class of GH secretagogues.
TL;DR: The present data suggest that this cessation of dorsal raphe unit activity is caused by the mechanism of disfacilitation resulting from the cessation of discharge of norepinephrine- or histamine-containing neurons during PS.
Abstract: Using in vivo extracellular unit recordings combined with microdialysis infusion in the cat, we found that the cessation of discharge of presumed serotonergic dorsal raphe neurons during paradoxical sleep (PS) was completely blocked by either histamine or phenylephrine, an alpha1 adrenoceptor agonist, but not by bicuculline, a GABA receptor antagonist. In addition, application of mepyramine, a specific H1 histamine receptor antagonist, or prazosin, a specific alpha1 adrenoceptor antagonist, suppressed the spontaneous discharge of raphe neurons during both quiet waking and sleep. The present data suggest that this cessation of dorsal raphe unit activity is caused by the mechanism of disfacilitation resulting from the cessation of discharge of norepinephrine- or histamine-containing neurons during PS.