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Changes in total amount of stage four sleep as a function of partial sleep deprivation.
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Comparing the effects of sleep loss after experimental sleep deprivation and in clinical patients.
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Effects of pre- or post-training paradoxical sleep deprivation on two animal models of learning and memory in mice.
The aim of the present study was to verify the effects of pre- or post-training paradoxical sleep (PS) deprivation in mice tested in the passive and the plus-maze discriminative avoidance tasks. Three-month-old Swiss male mice were placed in narrow platforms in a water tank for 72 h to prevent the occurrence of PS. Control animals were kept in the same room, but in their home cages. Before or after this period, the animals were submitted to the training session of one of the behavioral tasks. The test sessions were performed 3 and 10 days after the training. The animals that were PS-deprived before the training session showed retention deficits in the test sessions performed 3 days later in both tasks (decreased latency to enter the dark chamber of the passive avoidance apparatus or increased percent time spent in the aversive arm of the plus-maze discriminative avoidance apparatus). Animals that were PS deprived after the training session showed no differences from control animals in the test sessions performed 3 days after the training in any of the tasks, but showed passive and discriminative avoidance retention deficits in the test performed 10 days after the training. The results suggest that both pre- and post-training paradoxical sleep deprivation produce memory deficits in mice. However, these effects have different temporal characteristics.
Effect of sleep deprivation on the physiological status of rat testis.
The effect of alteration of central turnover of monoamines on the intratesticular mechanisms in the testis of rats was studied after REM sleep-deprivation. The reduction in the weights of ventral prostate, seminal vesicles and decreased activity of beta-glucuronidase in kidney reflected decreased availability of testosterone to the target organs. Decreased activities of lysosomal enzymes, acid phosphatase and beta-glucuronidase were associated with a decreased steroidogenic activity in the testis. The active mediation of lysosomal enzymes in the testicular function under altered condition was indicated.
Sleep-deprived mice show altered cytokine production manifest by perturbations in serum IL-1ra, TNFa, and IL-6 levels.
Serum cytokine and chemokine levels were examined in mice following 36 h of sleep deprivation, or after exposure to a known physical stressor (rotational stress). Significant changes in inflammatory cytokines/chemokines (IL-1beta, TNFalpha, IL-1ra, IL-6, and MIP-1beta, MCP-1) were observed following each manipulation, but qualitative and quantitative differences were seen. Interestingly, only physical stress was associated with measured increases in serum corticosterone levels, and with independent evidence (using in vitro immune allostimulation) for a generalized immunosuppression secondary to the experimental manipulation. Our data suggest that altered cytokine production following sleep perturbation occurs by a different mechanism from that (HPA axis) commonly attributed to stress per se.
The effects of chewing versus caffeine on alertness, cognitive performance and cardiac autonomic activity during sleep deprivation.
Chewing has been shown to alleviate feelings of sleepiness and improve cognitive performance during the day. This study investigated the effect of chewing on alertness and cognitive performance across one night without sleep as well as the possible mediating role of cardiac autonomic activity. Fourteen adults participated in a randomized, counterbalanced protocol employing a chewing, placebo and caffeine condition. Participants completed tasks assessing psychomotor vigilance, tracking, grammatical reasoning, alertness and sleepiness each hour across the night. All participants received either placebo or caffeine (200 mg), while the chewing condition also chewed on a tasteless and odorless substance for 15 min each hour. Heart rate (HR), root mean square of the successive differences in R-R intervals on the ECG (RMSSD), and preejection period (PEP) were simultaneously recorded. Alertness and cognitive performance amongst the chewing condition did not differ or were in fact worse when compared with placebo. Similarly, measures of HR and RMSSD remained the same between these two conditions; however, PEP was reduced in the later part of the night in the chewing condition compared with a relative increase for placebo. Caffeine led to improved speed and accuracy on cognitive tasks and increased alertness when compared with chewing. Relative increases in RMSSD and reductions in HR were demonstrated following caffeine; however, no change in PEP was seen. Strong associations between cardiac parasympathetic activity and complex cognitive tasks, as well as between subjective alertness and simpler cognitive tasks, suggest a differential process mediating complex versus simple cognitive performance during sleep deprivation.
Self-rated arousal concurrent with the antidepressant response to total sleep deprivation of patients with a major depressive disorder: a disinhibition hypothesis.
In view of the opposing theories regarding the arousing or de-arousing action of total sleep deprivation (TSD) in producing antidepressant effects, 23 patients with a major depressive disorder were deprived of a night's sleep twice weekly for two weeks, and self-rated their condition 38 times using von Zerssen's scale for depression and, concurrently, Thayer's Activation Deactivation Adjective Check List (AD ACL). Transient relief of depression after TSD, indicated by eight patients, was mimicked by their AD ACL scores, which revealed the same underlying factors as were found in Thayer's studies. TSD appears to be simultaneously arousing (giving more energy) and de-arousing (leading to less tension), while this response takes place against a background of increased tiredness/sleepiness. It is argued that TSD sets off a psychological disinhibition process on the basis of cerebral fatigue; in particular the prefrontal (orbital?) areas of the cerebral cortex may be implicated, possibly in relation to a dampening down of subcortical arousal systems.
Response to total sleep deprivation before and during treatment with fluvoxamine or maprotiline in patients with major depression--results of a double-blind study.
To test the hypothesis that the antidepressant effects of total sleep deprivation (TSD) are linked to the serotonergic and/or noradrenergic system the authors carried out a double-blind study (fluvoxamine versus maprotiline) in 42 inpatients with endogenous depression (ICD). Patients were randomized to a four-week treatment with either fluvoxamine (100-300 mg/day) or maprotiline (100-300 mg/day). In addition, patients underwent a TSD procedure before and after one week of antidepressant medication. There was a statistically significant reduction of depression ratings (HDRS) in both the fluvoxamine and maprotiline group. The day-1 response to TSD before antidepressive medication was not associated with a clear relationship to the outcome after four weeks of treatment with either fluvoxamine or maprotiline. On the other hand, the day-2 response to TSD was significantly correlated with a good outcome to subchronic treatment with maprotiline. Furthermore, the results of the authors' data suggest that a favorable short-term outcome of TSD may be connected to antidepressants enhancing the serotonergic neurotransmission. The global comparison between fluvoxamine and maprotiline revealed that the group of patients treated with fluvoxamine had a significantly higher efficiency index (CGI) than the maprotiline group; fluvoxamine was rated to be tolerated excellently in 70% of the patients whereas this percentage was only 43% in the maprotiline group. There was also significantly more vertigo and dry mouth in the maprotiline group whereas the fluvoxamine group was rated to have significantly more sleep disturbances during the trial.
Sleep deprivation response in seasonal affective disorder during a 40-h constant routine.
BACKGROUND: There are no controlled studies investigating the response of patients with seasonal affective disorder (SAD) to a total sleep deprivation (SD). METHODS: The clinical response to SD of patients with SAD in winter was investigated under the stringently controlled conditions of a 40-h constant routine protocol. RESULTS: 52% of the SAD patients (N=11 women) improved, using a mean of a multiple ratings. This is in the range of response found for non-seasonal major depression. In contrast, controls (N=8 women) showed less improvement of mood (29%). CONCLUSION: SAD patients respond to SD as do non-seasonal major depressives. The best discrimination of response was obtained in an observer rating (Clinical Global Impression: global severity improvement), and the morning values of two different self ratings (v. Zerssen depression scale, 100 mm VAS with the criterion of > or =10 mm improvement). LIMITATION: A more reliable estimate of the SD response rate in SAD patients would require a larger group. CLINICAL RELEVANCE: SAD patients do not differ from other subgroups of major depression in their response to SD, and therefore this is an additional treatment option to light therapy.
[Effect of sleep deprivation on visual evoked potentials and brain stem auditory evoked potentials in epileptics].
The article reports on the first study of the evoked activity of the brain in epileptic patients (n = 20) following sleep deprivation. An analysis of the data obtained has revealed a tendency to the shortening of the peak latent intervals of visual evoked potentials in the range of 100-200 mu sec and the V component and the interpeak interval III-V of evoked auditory trunk potentials in patients with temporal epilepsy. The phenomenon may indicate the elimination of stabilizing control involving the specific conductive pathways and, possibly, an accelerated conduction of a specific sensor signal.
Paradoxical sleep deprivation: effects on brain energy metabolism.
A study was made of brain nucleotides and glycolytic intermediates in paradoxical sleep (PS)-deprived and recovery-sleeping rats. It was observed that PS deprivation of 24 h produced a fall in glucose, glucose 6-phosphate and pyruvate in cerebral frontal lobes. After three hours of recovery sleep all values returned toward their predeprivational levels. In cerebellar hemispheres ATP was increased, while glucose 6-phosphate and pyruvate were decreased. After three hours of recovery sleep, glucose 6-phosphate was increased and pyruvate decreased, indicating restoration of glycogen and creatine phosphate respectively.
Caffeine and light effects on nighttime melatonin and temperature levels in sleep-deprived humans.
The effects of caffeine ingestion and exposure to bright light, both separately and in combination, on salivary melatonin and tympanic temperature were assessed in humans. Four treatments during a 45.5 h sleep deprivation period were compared: Dim Light-Placebo, Dim Light-Caffeine, Bright Light-Placebo and Bright-Light Caffeine. The Dim Light-Caffeine condition (200 mg twice each night) relative to the Dim Light-Placebo condition suppressed nighttime melatonin levels and attenuated the normal decrease in temperature. Combining caffeine ingestion with bright light exposure (> or = 2000 lux) suppressed melatonin and attenuated the normal nighttime drop in temperature to a larger degree than either condition alone; i.e. effects were additive. Circadian effects were also observed in that the amplitude and phase of the temperature rhythm were altered during treatment. These findings establish that the human melatonin system is responsive to caffeine. Other evidence suggests that caffeine may influence melatonin and temperature levels through antagonism of the neuromodulator adenosine.
Sleep deprivation hastens the antidepressant action of fluoxetine.
Among ten bipolar depressed patients admitted to our psychiatric ward, five patients were treated with fluoxetine alone and five subjects were treated with fluoxetine in association with total sleep deprivation (TSD) in order to evaluate the effect of the interaction between the administration of the serotonergic antidepressant compound fluoxetine and repeated cycles of TSD. Patients treated with fluoxetine plus repeated TSD showed a faster amelioration of depressive symptomatology compared with the other group. We discuss our findings hypothesizing an enhancement in dopaminergic and possibly in serotonergic transmission due to repeated TSD adding to the increase in serotonergic transmission due to fluoxetine medication.
Prolonged sleep-deprivation induced disturbed liver functions serum lipid levels, and hyperphosphatemia.
Sixty-four healthy young male volunteers were kept awake from 76 to 80 h. Blood tests conducted at the start and conclusion of the continuous sleep deprivation revealed an increase of 170% in mean SGOT, 58.5% in mean SGPT and 37.5% in mean plasma phosphorus levels. Triglyceride levels decreased by 16%, while HDL levels increased by 18% and the apoB/apoA ratio decreased by 12%. Morning plasma cortisol showed a significant increase during the experiment while evening cortisol showed a significant decrease. Morning T3 levels increased from the first to second day and decreased on the third day. There were no significant changes in other plasma electrolyte levels.
Inhibitory effect of GABAergic drugs in cocaine-induced genital reflexes in paradoxical sleep-deprived male rats.
The aim of this study was to seek whether GABAergic drugs were involved in the action of cocaine on spontaneous genital reflexes (penile erection-PE, and ejaculation-EJ) of paradoxical sleep-deprived (PSD) male rats. After a 4-day period of PSD, each group was administered with GABAergic drugs 1 h prior to cocaine and placed in observation cages. The administration of gamma-aminobutyric acid (GABA)-A agonist (muscimol, 2 and 3 mg/kg sc) reduced the number of animals displaying PE, whereas all doses tested of muscimol and bicuculline significantly reduced the frequency of PE. Pretreatment with the lower doses of GABA-B antagonist, phaclofen (1 and 2 mg/kg sc), also significantly reduced the percentage of rats showing PE; however, after the higher dose injection, the proportion of animals with PE was similar to those seen after vehicle pretreatment. Both GABA-B agonist and antagonist significantly reduced the PE frequency for all doses used compared with the vehicle group. There were no significant differences between control and GABA-A drugs in EJ behavior, whereas phaclofen 2 mg/kg pretreatment increased the ejaculatory latency. These data show that GABAergic compounds inhibited PE in male PSD rats suggesting that this inhibition points to a differential role of GABA receptor subtypes.
Effects of sleep deprivation on the postnatal development of visual-deprived cells in the cat's lateral geniculate nucleus.
1. Observations made by Wiesel and Hubel in kittens during the critical period have shown that monocular visual deprivation (MD) produces hypotrophic changes in the deprived layers of the LGN. Since, in addition to retinal inputs, the LGN also receives extraretinal inputs which are particularly active during REM sleep (a phase which is highly represented at birth), we performed experiments to find out whether total sleep deprivation (SD) interferes with the neuronal maturation in the LGN, thus modifying the susceptibility of LGN neurons to MD. 2. Ten groups of twin kittens were submitted to eyelid suture of one side at the age of 12 to 42 days after birth, and maintained into MD for periods of time which produced only slight or negligible changes in the deprived LGN layers. However, one of the twins in each group was allowed to sleep, while the other was submitted to 2 to 6 days of SD obtained by gentle handling during the last period of MD. At the end of the experiments cross-sectional areas of cell bodies were measured in the binocular segment of different layers of the LGN of both sides, at comparable levels. 3. MD, started 25 to 42 days after birth and continued for 11 to 23 days produced a slight but significant reduction of the mean cell area in the visual-deprived magnocellular ventral (C) and/or dorsal (A) layers of the contralateral LGN, but not in the middle (A1) layer of the ipsilateral LGN. This shrinkage, however, was most severe and involved also the layer A1 if kittens were also submitted to 5-6 days of SD during the last period of MD. There was also a tendency towards increased size in the nondeprived geniculate layers, probably due to an increased monocular visual experience resulting from an increased wake time in the light. However, the slight increase in cell size seen in these layers contrasted with the prominent increase in shrinkage of the visual-deprived layers after SD, indicating that this finding might have resulted from removing an influence of sleep. The effects of SD appeared to depend on the age of kittens (critical period) and the duration of MD. 4. In conclusion, shortly after birth, SD enhanced the structural abnormalities produced by monocular eyelid closure in the visual-deprived LGN layers. Since rhythmic discharges of pontine structures impinge on the LGN neurons during REM sleep, it is postulated that they could represent an endogenous source of stimulation leading to periodic read out of the synaptic connections between primary optic fibers and LGN neurons. This extraretinal input may thus collaborate with the retinal input to facilitate neuronal maturation of the LGN. The possibility that specific noradrenergic and cholinergic neurons, normally acting on the visual system during the sleep-waking cycle, intervene in the postnatal development of the LGN neurons has been discussed.
Combination of bright light and caffeine as a countermeasure for impaired alertness and performance during extended sleep deprivation.
Effects of four conditions (Dim Light-Placebo, Dim Light-Caffeine, Bright Light-Placebo and Bright Light-Caffeine) on alertness, and performance were studied during the night-time hours across 45.5 h of sleep deprivation. Caffeine (200 mg) was administered at 20.00 and 02.00 hours and bright-light exposure (> 2000 lux) was from 20.00 to 08.00 hours each night. The three treatment conditions, compared to the Dim Light-Placebo condition, enhanced night-time performance. Further, the combined treatment of caffeine and all-night bright light (Bright Light-Caffeine) enhanced performance to a larger degree than either the Dim Light-Caffeine or the Bright Light-Placebo condition. Beneficial effects of the treatments on performance were largest during the early morning hours (e.g. after 02.00 hours) when performance in the Dim Light-Placebo group was at its worst. Notably, the Bright Light-Caffeine condition was able to overcome the circadian drop in performance for most tasks measured. Both caffeine conditions improved objective alertness on the Maintenance of Wakefulness Test. Taken together, the above results suggest that the combined treatment of bright light and caffeine provides an effective intervention for enhancing alertness and performance during sleep loss.