Changes In REM Sleep Research Articles

Effects of acute and chronic treatment with trazodone, an antidepressant, on the sleep-wake activity in rats

Rats were treated with trazodone (2.5 or 10 mg kg −1) twice a day (at light and dark onset) for 11 days, after chronic injection of physiological saline. The sleep-wake activity was recorded for 24 h on the baseline day (saline), on trazodone days 1, 5 and 11, and also on day 12, when physiological saline was injected age (withdrawal day). Trazodone administration increased non-REM sleep. The enhancement of non-REM sleep was dose-related and more pronounced during the dark cycle. The promotion of non-REM sleep was enhanced during the chronic treatment. There were no consistent changes in REM sleep. Spectral analysis of the EEG revealed an increase in slow-wave activity after administration of the high dose (10 mg kg −1) of the drug. It is concluded that trazodone, a clinically effective antidepressant, has a non-REM sleep-promoting effect. It is speculated that the promotion of sleep by trazodone may be mediated by serotonergic mechanisms.

Early diagnostic differentiation of primary dementia from primary depressive syndromes in the aged--a contribution to the discussion of pseudodementia

The syndromes associated with dementia and depression in old age show a considerable overlap and even coincidence, not only for statistical reasons. Starting with a critical evaluation of the term "pseudodementia", possibilities for a differentiation of both types of syndromes by characteristics of clinical features and history and by additional investigations are shown. A critical review of the literature with focus on the differentiating properties of the following methods is given: neuropsychology and rating scales (e.g., "cortical" mediated versus motivational changes), neurophysiology (electroencephalography, EEG; evoked potentials, EP; event-related potentials, ERP), sleep physiology (REM-sleep changes; sleep deprivation results), neuroendocrinology (dexamethasone suppression test), neuroradiology (cranial computed tomography, CCT; magnetic resonance imaging, MRI) and especially the dynamic imaging methods of nuclear medicine (cerebral glucose metabolism with fluorodeoxyglucose and positron emission tomography, FDG-PET; cerebral blood flow (CBF) measurements with PET and single photon emission tomography, SPET). Developments during recent years concerning better imaging of early hippocampal lesions (MRI) or analysis of CBF--changes induced by activation methods may be very helpful. In conclusion, one can say that the diagnosis of dementia and depression remains primarily a clinical one that can be ascertained by means of valuable diagnostic tools.

Does Trampolining and Anaerobic Physical Fitness Affect Sleep?

The structure of nocturnal sleep of 16 volunteers, participating in the anaerobic sports of trampolining, dancing, and soccer, was monitored by means of polygraphic recordings. Since trampolining requires the acquisition of unfamiliar patterns of motor coordination, it can be considered as a special form of motor learning, whereas the acquisition of motor skills specific for dancing and soccer can be linked with motor patterns of normal biped locomotion. According to this view, an experimental group of 8 volunteers was formed; they participated in a training course of trampolining. In addition, a control group of 8 subjects was recruited, who engaged in one of the other two anaerobic sports. Subjects who had acquired new motor skills during a 13-wk. program in trampolining showed a statistically significant increase in REM-sleep. By contrast, the 8 subjects of the control group showed no considerable changes in REM-sleep. This suggests that efforts in acquiring new and complex motor patterns activate processes specifically involved in the generation of REM stage during nocturnal sleep.

DOES TRAMPOLINING AND ANAEROBIC PHYSICAL FITNESS AFFECT SLEEP?

The structure of nocturnal sleep of 16 volunteers, participating in the anaerobic sports of trampolining, dancing, and soccer, was monitored by means of polygraphic recordings. Since trampolining requires the acquisition of unfamiliar patterns of motor coordination, it can be considered as a special form of motor learning, whereas the acquisition of motor skills specific for dancing and soccer can be linked with motor patterns of normal biped locomotion. According to this view, an experimental group of 8 volunteers was formed; they participated in a training course of trampolining. In addition, a control group of 8 subjects was recruited, who engaged in one of the other two anaerobic sports. Subjects who had acquired new motor skills during a 13-wk. program in trampolining showed a statistically significant increase in REM-sleep. By contrast, the 8 subjects of the control group showed no considerable changes in REM-sleep, This suggests that efforts in acquiring new and complex motor patterns activate processes specifically involved in the generation of REM stage during nocturnal sleep.

Lifetime monoamine oxidase inhibition and sleep

The effects of clorgyline, a type A monoamine oxidase (MAO) inhibitor, on the sleep of the rat were examined after subacute and lifetime administration. When 2 mg/kg/24 hours were given for 60 hours, type A MAO was inhibited by 92% and a significant reduction in REM sleep time was noted. When fetal rats were exposed to maternal dosage of 1 mg/kg/24 hours and then received this dose from one to 6 weeks postnatally, type A MAO was inhibited by 99%, but there were no alterations in the EEG sleep stages. In summary, subacute administration of clorgyline resulted in decreases in both Type A MAO and REM sleep; during chronic administration in a developing animal, Type A MAO was again decreased, but there was no corresponding changes in REM sleep.

Bed-time food supplements and sleep: Effects of different carbohydrate levels

Blood glucose levels were altered during sleep by means of manipulating carbohydrate (CHO) intake through bed-time food supplements. Protein and fat intake were minimally affected. Subjects underwent all conditions in a balanced design. A high CHO condition resulted in significantly reduced stages 1 + 0 sleep over the whole night and significantly increased REM sleep during the first half of the night; there seemed to be a reciprocity between these two changes. High CHO also produced a whole-night significant decrease in stages 4 sleep, which persisted into the recovery night. Few significant differences between the other conditions of low and zero CHO were found. Sleep onset was not affected. It was concluded that relatively high blood glucose levels were required to alter sleep, and perhaps lead to more ‘restful’ sleep. The present findings were similar to those of related studies. The REM sleep changes were discussed in relation to increases in brain serotonin synthesis mediated by elevated blood glucose levels.

MAO activity and EEG sleep in primary depression

Platelet monoamine oxidase (MAO) activity and electroencephalographic (EEG) sleep measures were examined in 56 drug-free hospitalized patients with primary depression as defined by the Research Diagnostic Criteria. The group included 35 females and 21 males with a mean age of 42.6±1.4 years. Platelet MAO and EEG sleep data were compared for the group as a whole and seperately for the unipolar, bipolar, male, and female subgroups. No significant relationships could be demonstrated for the entire group or for the unipolar, male, or female subgroups. However, an inverse relationship between MAO activity and REM sleep percent was noted in the bipolar subgroup ( p<0.02). While changes in REM sleep have been relatively firmly established in primary depression, the relationship of MAO to depression and to REM sleep remains unclear.

Individual variations in the effects of flurazepam, clorazepate, L-dopa and thyrotropin-releasing hormone on REM sleep in man

The comporative effects of flurazepam, clorazepate, L-dopa, and thyrotropin-releasing hormone (TRH) on REM sleep were investigated in normal, healthy adults. A single dose of each drug was given orally to the subjects 30 min before bedtime. A dose of 30 mg flurazepam significantly decreased REM sleep-time when compared to the mean baseline record. No change was noted in REM sleep-time on the clorazepate (15 mg) night, L-dopa (1000 mg) night, or TRH (2 mg) night, when compared to the mean baseline record. Because large individual variations were found in REM sleep time on each drug night, and in percentage increase in REM sleep following partial differential REM deprivation (PDRD), correlation was investigated between them. The percentage decrease in REM sleep during flurazepam was found to have a significant negative correlation with the percentage increase in REM sleep after PDRD in individual subjects. Although there was no significant change in REM sleep on TRH night when compared to the mean baseline record, a similar significant negative correlation was noted. On the L-dopa night, there was a tendency toward a negative correlation between them. No significant correlation was noted on the clorazepate night.

REM sleep in primary depression: A computerized analysis

REM sleep in 35 inpatients with primary depression was automatically analyzed for 7 consecutive nights during placebo administration. For the total night of sleep, as well as each individual REM period, the number of REMs, their total voltage integral over time, the sum of their durations and the average REM size were automatically calculated. Validity of these automated REM measures was established by significant correlations with manually scored REM measures. Changes in REM sleep across the night were also investigated. Similar to findings in normal subjects, REM time did not change from REM period to REM period. Average REM size increased significantly from REM period 2–3 and 3–4. Contrary to what is seen in normal subjects, REM frequency was high during the first REM period, significantly decreased from the first to second REM period and then remained constant. Finally, a significant inverse correlation between REM frequency for the first REM period and REM latency was noted. This pattern of REM sleep is interpreted as indicating a high pressure for phasic REM at the beginning of the night which is dissipated by the first REM period.

969 SLEEP STATE AND MATURATION OF CO2 SENSITIVITY IN THE PREMATURE PRIMATE

Sleep apnea and altered CO2 sensitivity have been implicated in the pathophysiology of SIDS. To investigate the hypothesis that sleep state and postnatal maturation influence minute ventilation and steady state CO2 sensitivity, 7 healthy premature M. nemestrina were studied serially in the first 3 weeks of life. VE/Kg in room air, 2,3,4, and 5% CO2 was measured via nasal wrongs and hot wire anemometer and arterial gases were sampled in 3 animals after a steady state was attained. Sleep state was assessed from EEG, EOG, EMG and respiratory pattern. Baseline VE/Kg and VT/Kg increased and f decreased in REM and NREM sleep with increasing postnatal age (p<.05), but there were no differences in VE/Kg between the 2 states at each age. VE/Kg increased following inhalation of CO2 in each state at each postnatal age, but there were no significant differences in CO2 sensitivity between NREM and REM sleep. In NREM sleep CO2 sensitivity increased progressively with increasing postnatal age (p<.025) whereas in REM sleep this maturational increase in slope was not observed (p>.4). The CO2 ventilatory response curve shifted to the left in both states with increasing age. These results suggest that there is a sleep state specific difference in postnatal maturation of CO2 sensitivity - a progressive increase in NREM sleep and no significant change in REM sleep. Failure of this normal maturational increase in NREM sleep may be important to the pathophysiology of SIDS.

Individual variations in response of human REM sleep to amitriptyline and haloperidol

The effect of amitriptyline and haloperidol on REM sleep was investigated in healthy human adults, with special attention to individual variations in these drugs' effects. In addition, an investigation was made of the rebound elevation of REM sleep occurring on the following night of partial differential REM deprivation (PDRD), again with emphasis being placed on individual variations in that effect. The administration of amitriptyline in a single oral dose of 25 mg was followed by an inhibition of REM sleep in all subjects. The per cent decrease in REM sleep was found to have a significant negative correlation with the per cent increase in REM sleep following PDRD in individual subjects. The amount of REM sleep during the recovery night following the night of amitriptyline medication tended to correlate with the per cent increase in REM sleep following PDRD in individual subjects. Haloperidol in a single oral dose of 1.5 mg caused REM sleep to augment in some subjects but inhibit in others. A significant correlation was noted to exist between drug-induced change in REM sleep and the per cent increase in REM sleep following PDRD.