Effects of circadian phase and duration of sleep deprivation on sleep and EEG power spectra in the cat

Lancel, Marike; Riezen, H. van; Glatt, A.

doi:10.1016/0006-8993(91)91123-i

Cited by 56 publications

(35 citation statements)

References 20 publications

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“…During SWS, ␦ activity is maximal at the beginning of the sleep period and declines progressively during the sleep period (Rosenberg et al, 1976;Borbely et al, 1981;Lancel et al, 1991). After sleep deprivation, ␦ activity is enhanced, especially in the first part of deprived sleep (Rosenberg et al, 1976;Borbely et al, 1981;Tobler and Borbely, 1986;Lancel et al, 1991).…”

Section: Discussionmentioning

confidence: 96%

“…Correlations between VTA GABA neuronal activity and electrocortical activity after sleep deprivation Sleep deprivation produces an increase in ␦ wave power during deprived sleep relative to normal sleep (Rosenberg et al, 1976;Borbely et al, 1981;Lancel et al, 1991). Because VTA GABA neuron firing rate decreased during SWS and increased during REM relative to AW, we sought to determine whether VTA GABA neuron activity correlated with the changes in EEG power produced by sleep deprivation.…”

Section: Correlations Between Vta Gaba Neuronal Activity and Electrocmentioning

confidence: 99%

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Discharge Profiles of Ventral Tegmental Area GABA Neurons during Movement, Anesthesia, and the Sleep–Wake Cycle

2001

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Although mesolimbic dopamine (DA) transmission has been implicated in behavioral and cortical arousal, DA neurons in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) are not significantly modulated by anesthetics or the sleep-wake cycle. However, VTA and SN non-DA neurons evince increased firing rates during active wakefulness (AW) and rapid eye movement (REM) sleep, relative to quiet wakefulness. Here we describe the effects of movement, select anesthetics, and the sleep-wake cycle on the activity of a homogeneous population of VTA GABA-containing neurons during normal sleep and after 24 hr sleep deprivation. In freely behaving rats, VTA GABA neurons were relatively fast firing (29 Ϯ 6 Hz during AW), nonbursting neurons that exhibited markedly increased activity during the onset of discrete movements. Adequate anesthesia produced by administration of chloral hydrate, ketamine, or halothane significantly reduced VTA GABA neuron firing rate and converted their activity into phasic 0.5-2.0 sec ON/OFF periods. VTA GABA neuron firing rate decreased 53% during slow-wave sleep (SWS) and increased 79% during REM, relative to AW; however, the discharging was not synchronous with electrocortical ␣ wave activity during AW, ␦ wave activity during SWS, or ␥ wave activity during REM. During deprived SWS, there was a direct correlation between increased VTA GABA neuron slowing and increased ␦ wave power. These findings indicate that the discharging of VTA GABA neurons correlates with psychomotor behavior and that these neurons may be an integral part of the extrathalamic cortical activating system. Key words: ventral tegmental area; anesthesia; slow-wave sleep; rapid eye movement sleep; sleep deprivation; GABA; cortical activationThe ventral tegmental area (VTA) is the source of dopamine (DA)-containing neurons that project to structures in the ventral striatum, hypothalamus, and prefrontal association cortex, known collectively as the mesocorticolimbic DA system. This neural circuit has been implicated in mediating several motivated behaviors (for review, see Mogenson, 1987;Wise and Rompre, 1989). In this context, midbrain DA neurons in the VTA and substantia nigra pars compacta (SNc) respond to alerting, activating, and reward-related stimuli (Trulson and Preussler, 1984;Schultz, 1986;Freeman and Bunney, 1987;Schultz et al., 1993). Although mesolimbic DA transmission has been implicated in behavioral (for review, see Kalivas et al., 1993) and electrocortical (Radulovacki et al., 1979;Kropf et al., 1989;Kropf and Kuschinsky, 1991; Sebban et al., 1999a,b) activation, the firing rate of DA neurons in the VTA and SNc is not significantly modulated by the sleepwake cycle or anesthetics (Miller et al., 1983;Steinfels et al., 1983). However, VTA and SNc non-DA neurons evince increased firing rates during active wakefulness (AW) and rapid eye movement (REM) sleep, relative to quiet wakefulness (QW) (Miller et al., 1983).Although some progress has been made in elucidating the role of DA neurons in arousal ...

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Section: Discussionmentioning

confidence: 96%

Section: Correlations Between Vta Gaba Neuronal Activity and Electrocmentioning

confidence: 99%

Discharge Profiles of Ventral Tegmental Area GABA Neurons during Movement, Anesthesia, and the Sleep–Wake Cycle

2001

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“…The hypothesis that there should be conservation of sleep loss-dependent changes in gene expression was influenced by the observation that EEG SWA is sleep history-dependent in a number of mammalian species (Tobler and Jaggi, 1987, Trachsel et al, 1989, Dijk et al, 1990, Lancel et al, 1991, Franken et al, 2001. If sleep history-dependent changes in SWA reflect a restorative process that is manifest at the level of gene expression in the Cx, RS should enhance this molecular response.…”

Section: Discussionmentioning

confidence: 99%

Gene expression in the rat brain during sleep deprivation and recovery sleep: an Affymetrix GeneChip® study

et al. 2006

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Previous studies have demonstrated that macromolecular synthesis in the brain is modulated in association with the occurrence of sleep and wakefulness. Similarly, the spectral composition of electroencephalographic activity that occurs during sleep is dependent on the duration of prior wakefulness. Since this homeostatic relationship between wake and sleep is highly conserved across mammalian species, genes that are truly involved in the electroencephalographic response to sleep deprivation (SD) might be expected to be conserved across mammalian species. Therefore, in the rat cerebral cortex, we have studied the effects of SD on the expression of immediate early gene (IEG) and heat shock protein (HSP) mRNAs previously shown to be upregulated in the mouse brain in SD and in recovery sleep (RS) after SD. We find that the molecular response to SD and RS in the brain is highly conserved between these two mammalian species, at least in terms of expression of IEG and HSP family members. Using Affymetrix Neurobiology U34 GeneChips ® , we also screened the rat cerebral cortex, basal forebrain, and hypothalamus for other genes whose expression may be modulated by SD or RS. We find that the response of the basal forebrain to SD is more similar to that of the cerebral cortex than to the hypothalamus. Together, these results suggest that sleep-dependent changes in gene expression in the cerebral cortex are similar across rodent species and therefore may underlie sleep historydependent changes in sleep electroencephalographic activity. KeywordsTaqman analysis; sleep deprivation; immediate early genes; basal forebrain; cerebral cortex; hypothalamus HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptSleep is a homeostatic process in that the time spent asleep and the continuity of sleep states are directly related to the duration of prior wakefulness. Although sleep duration and the time spent in each of its stages are parameters commonly measured in sleep studies, sleep also has an intensity dimension, measurable by slow wave activity (SWA) in the electroencephalogram (EEG) during non-rapid eye movement (NREM) sleep. The amplitude of EEG SWA is directly proportional to the duration of prior wake and consequently has been proposed as a marker for the homeostatic regulation of sleep in mammals (Borbely and Achermann, 2000). Accordingly, sleep need, measurable as EEG SWA once sleep is initiated, is thought to accrue during wakefulness. Conversely, the decline of EEG SWA amplitude across a sleep bout is thought to reflect the diminution of the sleep-dependent "Process S" that reflects recovery from prior waking activities.The temporal dynamics of the sleep-dependent discharge of sleep need (reflected in the decay of the sleep-dependent Process S) is conserved among genetically distinct rodent strains (Franken et al., 2001). The conserved nature of Process S supports the concept that EEG SWA may be an electrophysiological marker of restorative neurochemical processes that occur during...

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“…In advance to REMS, delta activity falls rapidly and is mini mal during REMS. In humans [7] and rats [8], the rise rate of delta activity as well as the plateau level within a NREMS episode decrease throughout the predominant sleep period, whereas in the cat the rise rate and the maxi mal level reached remain unchanged over the 12-hour dark period [12], Under undisturbed conditions, the EEG power densi ties within REMS do not change systematically over the sleep period or over 24 h in, e.g., hamsters [4], rats [3], cats [11] and rabbits [6], In humans, only a weak decreas ing tendency in the course of a normal night sleep has been reported in a small frequency range, centered at 15 Hz [1,7], This suggests that, in contrast to NREMS, REMS lacks an intensity dimension.…”

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confidence: 99%

“…It is still obscure whether these enhancements reflect a circadian rhythm or sleep satiation. In mammals that do not exhibit a strong circadian sleep-wake pattern, like the rabbit [6] and the cat [11], only minor variations in EEG power densities occur over the 24-hour day. This probably results from the absence of long, uninterrupted periods of wakefulness.…”

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confidence: 99%

Cortical and Subcortical EEG in Relation to Sleep-Wake Behavior in Mammalian Species

Lancel

1993

Neuropsychobiology

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In humans and several other mammals, a quantitative EEG analysis has been used to study the regulation of sleep-wake behavior. In all mammalian species studied, cortical EEG recorded during non-REM sleep (NREMS) is characterized by the occurrence of spindles and high voltage, slow waves (0.5-4.0 Hz). Furthermore, slow-wave activity (SWA) is low at the beginning of a NREM episode and it rises in the course of a NREM episode. The rise rate and the maximal level of SWA are a monotonic function of the duration of prior wake-fulness. During REMS, cortical EEG typically exists of low-voltage, mixed frequencies and, in some animals, a prominent theta rhythm is superimposed. Only after sleep deprivation in some species does cortical EEG within REMS change. Especially, the EEG activity during wakefulness depends considerably on the behavioral state, on the electrode location and on the species. On average, cortical EEG within wakefulness consists of low-voltage, mixed frequencies. The few studies done on subcortical EEG clearly show that the electrical activity differs highly between brain regions and between species. However, two recent studies, in which a spectral analysis of subcortical EEG was made, showed that, at least in humans and cats, the changes occurring in subcortical EEG associated with changes in sleep-wake behavior parallel the general characteristics of cortical EEG described above.

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Effects of circadian phase and duration of sleep deprivation on sleep and EEG power spectra in the cat

Cited by 56 publications

References 20 publications

Discharge Profiles of Ventral Tegmental Area GABA Neurons during Movement, Anesthesia, and the Sleep–Wake Cycle

Discharge Profiles of Ventral Tegmental Area GABA Neurons during Movement, Anesthesia, and the Sleep–Wake Cycle

Gene expression in the rat brain during sleep deprivation and recovery sleep: an Affymetrix GeneChip® study

Cortical and Subcortical EEG in Relation to Sleep-Wake Behavior in Mammalian Species

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