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PubMed2002

Topographical changes in N1-P2 amplitude upon awakening from recovery sleep after slow-wave sleep deprivation.

OBJECTIVES: To assess auditory evoked potentials (AEPs) before sleep and upon 3 awakenings during an undisturbed baseline night and to compare them to AEPs during a night characterized by a recuperative increase in the amount of slow-wave sleep (SWS) as a consequence of two consecutive nights of selective SWS deprivation. METHODS: Ten male subjects slept in the laboratory for 6 consecutive nights. The first 2 nights were undisturbed. The 3rd night was considered as baseline. During the 4th and 5th nights, selective SWS deprivation was obtained by means of acoustic stimulation. The 6th night was a recovery. The data reported here were collected during the baseline and the recovery night. Subjects were awakened 3 times: after 2 h, 5 h (nocturnal awakenings) and 7.5 h (final morning awakening) of sleep, respectively. All the awakenings were carried out from stage 2. The AEP recordings were carried out in bed, while subjects were performing a simple auditory reaction time task. RESULTS: The amplitude of the N1-P2 complex decreased upon the first awakening of the baseline night as compared to pre-sleep wakefulness levels; during the recovery night, the decrease of N1-P2 amplitude was present also upon the second and final awakening. N1 latency increased upon the two nocturnal awakenings regardless of the night, while P2 latency was not affected. Moreover, the N1-P2 amplitude increased during recovery at the frontal midline derivation as compared to baseline, while it decreased at Pz and Oz. CONCLUSIONS: The N1-P2 amplitude and, to a lesser extent, the N1 latency, are sensitive in showing a state of brain deactivation during the sleep-wake transition. The decrease of N1-P2 amplitude at the parieto-occipital locations during recovery is coherent with the hypothesis of a functional link between SWS amount and cortical hypoarousal upon awakening. The unexpected increase of the same variable at Fz can be interpreted as the effect of a compensatory effort of the frontal areas for the increased homeostatic drive for sleep during the recovery night.

Adult↗
PubMed1991

Short-term REM sleep deprivation increases acetylcholinesterase activity in the medulla of rats.

Involvement of cholinergic ponto-medullary brainstem mechanism regulating rapid eye movement (REM) sleep is known. Recently it was found that though short term REM deprivation influenced brainstem neuronal excitability, the activity of the brainstem acetylcholinesterase was not affected until after 96 h deprivation. Therefore, it was hypothesized that short-term REM deprivation might influence acetylcholinesterase in a restricted brainstem region. Results of this study show that the enzyme activity increased only in the medulla after 24 and 48 h REM deprivation. The flower pot technique was used for depriving the experimental rats of REM sleep. Suitable control experiments were conducted to rule out the possibility of non-specific effects. Thus, the medullary cholinergic mechanism probably is more important for REM.

Acetylcholinesterase↗
PubMed1989

Avoidance performance in rat enhanced by postlearning paradoxical sleep deprivation.

This series of experiments investigates possible relations between increases in paradoxical sleep (PS), persisting for several days after an avoidance training, and improvement of retention performance that occurred 3 days following partial training in a brightness discrimination Y-maze shock-avoidance task. Sprague-Dawley rats were trained in the Y-maze and PS deprived for 24 h either immediately or 24, 48, or 72 h following initial training. Contrary to what was expected, the results indicated that PSD immediately following the training session enhanced the avoidance performance after a 7-day retention interval. PSD at later times had no effect. Experiment 2 indicated that this effect was obtained only for PS-deprived animals and not for those placed in the PSD situation, but on larger platforms. Thus enhancement of the avoidance performance was not due to increases in stress or arousal caused by PSD-associated factors. Experiment 3 showed that the facilitative effect of a non-delayed 24-h PSD was obtained immediately thereafter as well as 24 h later, demonstrating that this effect was not due to any PS rebound which might have occurred following the PSD. Alternative explanations for these unexpected results are discussed.

Animals↗
PubMed2006

Differential effects of chronic partial sleep deprivation and stress on serotonin-1A and muscarinic acetylcholine receptor sensitivity.

Disrupted sleep and stress are often linked to each other, and considered as predisposing factors for psychopathologies such as depression. The depressed brain is associated with reduced serotonergic and enhanced cholinergic neurotransmission. In an earlier study, we showed that chronic sleep restriction by forced locomotion caused a gradual decrease in postsynaptic serotonin-1A receptor sensitivity, whilst chronic forced activity alone, with sufficient sleep time, did not affect receptor sensitivity. The first aim of the present study was to examine whether the sleep loss-induced change in receptor sensitivity is mediated by adrenal stress hormones. The results show that the serotonin-1A receptor desensitization is independent of adrenal hormones as it still occurs in adrenalectomized rats. The second aim of the study was to establish the effects of sleep restriction on cholinergic muscarinic receptor sensitivity. While sleep restriction affected muscarinic receptor sensitivity only slightly, forced activity significantly hypersensitized the muscarinic receptors. This hypersensitization is because of the stressful nature of the forced activity protocol as it did not occur in adrenalectomized rats. Taken together, these data confirm that sleep restriction may desensitize the serotonin-1A receptor system. This is not a generalized effect as sleep restriction did not affect the sensitivity of the muscarinic cholinergic receptor system, but the latter was hypersensitized by stress. Thus, chronic stress and sleep loss may, partly via different pathways, change the brain into a direction as it is seen in mood disorders.

Adrenal Glands↗
PubMed1987

Variations in nuchal muscle tonus following paradoxical sleep deprivation in the rabbit.

Although tonic inhibition of nuchal or facial musculature is considered an intrinsic component of paradoxical sleep (PS) in mammals, this inhibition is either absent or greatly attenuated in the rabbit. To further explore the characteristics of this phenomenon in this species, variations in quantified nuchal muscle activity were examined before, during and following 24 h of PS deprivation. It was postulated that if the substrate for PS-associated tonic electromyogram (EMG) inhibition is present, this procedure--which is known to affect both tonic and phasic components of PS--might enhance such inhibition. For these investigations chronically implanted rabbits (electroencephalographic, eye movement and nuchal muscle placements) were recorded continuously for 5 consecutive days (two day baseline, one day deprivation, two day recovery). Muscle activity was quantified by resetting integration techniques and comparisons made of activity levels before, during and after PS episodes across conditions. The deprivation procedure significantly reduced the amount of PS relative to baseline values, and a significant PS increase (rebound) occurred during postdeprivation recordings. Across-condition EMG-related effects included the corroboration of previous reports of an absence of nuchal atonia during PS, a significant diurnal variation in EMG activity--with greater activity occurring during the dark portion of the light-dark cycle, and enhanced activity immediately following PS episodes relative to either pre-PS or PS levels. Deprivation-related changes in quantified EMG activity included a pre-PS decrease during both the last 12 h of deprivation and the initial 12 h of recovery sleep, and an enhancement of EMG activity during PS.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Infant stress and sleep deprivation as an aetiological basis for the sudden infant death syndrome.

SIDS is almost invariably sleep-related. Viable syndrome aetiology must be compatible with its many epidemiologically diverse risk factors, each of which directly or indirectly associates with the creation of psychological and/or physiological infant stress, and the subsequent disruption of normal, contented sleep. During essential deep 'rebound' recovery sleep, arousal ability and upper airway muscle tone decrease further to that in normal sleep, with subsequent upper airway obstruction. When stress impact causes sufficient sleep disruption and physiological fatigue, a failure to arouse and so restore sufficient tone to overcome such obstruction results in sudden, unexpected death. SIDS has therefore many causes which share a final lethal mechanical pathway. Evidence is presented for obstructive apnoea during sleep as being the primary syndrome death mode, for sleep disruption, reduced arousal ability, and infant stress in SIDS, and for risk factor association with the creation of this stress. Specific infant vulnerability in the first 6 months of life to stress predominantly related to total dependency on a carer for gratification of need, and to obstructive sleep apnoea due to normal anatomical, physical, and respiratory immaturity, including rapid physiological fatigue, and peaks in sleep and thermal stress vulnerability, are discussed. Further reasons for the limited age period of SIDS, and for reduced neonatal risk, are given. Prone sleeping risk can relate to positional airway obstruction during normal sleep without prior infant stress. Much of SIDS aetiology appears to concern factors related to socio-economic deprivation and subsequent sub-optimal infant care.

Airway Obstruction↗
PubMed1995

REM sleep deprivation treatment enhances the effect of clozapine in the forced swimming test.

1. Effect of REM sleep (REMs) deprivation treatment on clozapine response in the forced swimming test was investigated. 2. Clozapine significantly increased the swimming activity in REMs-deprived mice at a dose of 5 mg/kg (i.p.) which did not affect the activities in the control groups. 3. Physostigmine (0.3 mg/kg, i.p.), an acetylcholinesterase inhibitor, blocked the increasing effect of 5 mg/kg clozapine on swimming activity in REMs-deprived animals. 4. These results suggest that the REMs deprivation treatment-induced enhancement of effect of clozapine on swimming activity is mediated by the functional change of central cholinergic system following the treatment.

Animals↗