Modulation of rapid eye movement sleep in humans by drugs that modify monoaminergic and purinergic transmission

Nicholson, A. N.; Belyavin, A.; Pascoe, Peta A.

doi:10.1016/0893-133x(89)90016-x

Cited by 37 publications

(26 citation statements)

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“…These drugs usually lead to an immediate and sustained suppression of REM sleep in the range of 50% of baseline values [32][33][34], Furthermore short-wavesleep-inducing properties of the magnitude as observed with carbamazepine have not been described for classical antidepressants like clomipramine [35] or amitriptyline [36], However, neuroendocrine and sleep EEG data from the present study suggest some similarities with lithium, which is also used as a prophylactic treatment in affective disorders.…”

Section: Discussionmentioning

confidence: 42%

The Effect of Carbamazepine on Endocrine and Sleep EEG Variables in a Patient with 48-Hour Rapid Cycling, and Healthy Controls

et al. 1993

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Carbamazepine treatment of a patient with 48-hour rapid cycling led to a dampening of mood cycling, and prolonged rapid eye movement (REM) sleep latency. No effect on central α-receptors as measured by growth hormone (GH) secretion after clonidine stimulation or on spontaneous 48-hour GH secretion was observed. In 12 healthy subjects given 400 mg carbamazepine daily for a period of 5 days, improved sleep continuity and increased slow-wave sleep occurred with treatment. REM sleep percentage and REM latency remained uninfluenced, whereas REM density decreased. GH secretion after clonidine stimulation was not altered. Data from the single-case longitudinal study emphasize that carbamazepine is effective in treating rapid-cycling affective psychosis. Furthermore, neuroendocrine and sleep EEG data from the study in healthy subjects indicate a different profile of action for carbamazepine compared to most other antidepressants or antimanic drugs.

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Section: Discussionmentioning

confidence: 42%

The Effect of Carbamazepine on Endocrine and Sleep EEG Variables in a Patient with 48-Hour Rapid Cycling, and Healthy Controls

et al. 1993

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“…Stage REM might then occur randomly with a probability depending on the momentary REM and non-REM tendencies. This concept could explain the sporadic observation of SOREMPS at the beginning of a sleep cycle, could include the discussed phenomena following forced awakenings and might also serve as an explanation for the so-called skipped REM episodes [23,36,37].…”

Section: Discussionmentioning

confidence: 99%

“…Besides the momentary REM pressure, a variety of parameters can influence this choice [17 -21]. Once the brain has decided for nonREM sleep, the system usually remains in this condition for at least some 30 min [3,5,22,23].…”

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confidence: 99%

Is the nonREM–REM sleep cycle reset by forced awakenings from REM sleep?

Grözinger

Beersma²,

Fell

et al. 2002

Physiology & Behavior

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In selective REM sleep deprivation (SRSD), the occurrence of stage REM is repeatedly interrupted by short awakenings. Typically, the interventions aggregate in clusters resembling the REM episodes in undisturbed sleep. This salient phenomenon can easily be explained if the nonREM -REM sleep process is continued during the periods of forced wakefulness. However, earlier studies have alternatively suggested that awakenings from sleep might rather discontinue and reset the ultradian process. Theoretically, the two explanations predict a different distribution of REM episode duration.We evaluated 117 SRSD treatment nights recorded from 14 depressive inpatients receiving low dosages of Trimipramine. The alarms were triggered by an automatic mechanism for the detection of REM sleep and had to be canceled by the subjects themselves. The REM episodes were determined as in undisturbed sleep-they had to include the remaining REM activity and were separated by 30 min without REM epochs. The frequency histogram of REM episodes declined exponentially with episode duration for each of the first four sleep cycles. The duration of nonREM intervals revealed bimodal distributions. These results were found consistent with the model assuming a reset of the ultradian cycle upon awakening. Whether REM or nonREM activity is resumed on return to sleep can be modeled by a random decision whereby the probability for REM sleep might depend on the momentary REM pressure. D

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“…The analysis was based on the sleep recordings from 10 subjects for placebo nights from the series of drug studies described in Nicholson et al (1989). The subjects were selected as those for whom 10 or more such nights were available.…”

Section: Methodsmentioning

confidence: 99%

“…Belyavin and Nicholson 1987;Nicholson et al 1989) suggest that while the REM cycle is clearly reproducible, there is a substantial stochastic element determining both onset and duration of REM sleep. The bimodality of the distribution of the latency to REM under some circumstances, combined with the general cyclical appearance of REM episodes, supports the idea that a regular trigger is at least partially responsible for REM entry.…”

Section: Introductionmentioning

confidence: 99%

The duration of REM sleep episodes in normal sleep

Belyavin¹

1992

Journal of Sleep Research

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Modulation of rapid eye movement sleep in humans by drugs that modify monoaminergic and purinergic transmission

Cited by 37 publications

References 0 publications

The Effect of Carbamazepine on Endocrine and Sleep EEG Variables in a Patient with 48-Hour Rapid Cycling, and Healthy Controls

The Effect of Carbamazepine on Endocrine and Sleep EEG Variables in a Patient with 48-Hour Rapid Cycling, and Healthy Controls

Is the nonREM–REM sleep cycle reset by forced awakenings from REM sleep?

The duration of REM sleep episodes in normal sleep

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