The S-Deficiency Hypothesis of Depression and the Two-process Model of Sleep Regulation

Borbély, A A

doi:10.1055/s-2007-1017069

Cited by 157 publications

(118 citation statements)

References 11 publications

(20 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Shortly after the first description of the two-process model of sleep-wake regulation, it was hypothesized that in depressed patients the homeostatic regulation might be deficient as reflected in a lower build-up of sleep pressure during wakefulness (15). A key candidate mediating both the homeostatic process and the antidepressant effect is adenosine.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Recovery sleep after extended wakefulness restores elevated A ₁ adenosine receptor availability in the human brain

Elmenhorst

Hennecke

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Adenosine and functional A 1 adenosine receptor (A 1 AR) availability are supposed to mediate sleep-wake regulation and cognitive performance. We hypothesized that cerebral A 1 AR availability after an extended wake period decreases to a well-rested state after recovery sleep. [ 18 F]CPFPX positron emission tomography was used to quantify A 1 AR availability in 15 healthy male adults after 52 h of sleep deprivation and following 14 h of recovery sleep. Data were additionally compared with A 1 AR values after 8 h of baseline sleep from an earlier dataset. Polysomnography, cognitive performance, and sleepiness were monitored. Recovery from sleep deprivation was associated with a decrease in A 1 AR availability in several brain regions, ranging from 11% (insula) to 14% (striatum). A 1 AR availabilities after recovery did not differ from baseline sleep in the control group. The degree of performance impairment, sleepiness, and homeostatic sleep-pressure response to sleep deprivation correlated negatively with the decrease in A 1 AR availability. Sleep deprivation resulted in a higher A 1 AR availability in the human brain. The increase that was observed after 52 h of wakefulness was restored to control levels during a 14-h recovery sleep episode. Individuals with a large increase in A 1 AR availability were more resilient to sleep-loss effects than those with a subtle increase. This pattern implies that differences in endogenous adenosine and A 1 AR availability might be causal for individual responses to sleep loss.S leep loss is known to impair almost every aspect of cognition, such as learning (1), long-term memory consolidation (2), attention and psychomotor vigilance (PVT) (3), and executive functions (4), including decision making (5) and emotional control (6). Sleep deprivation further typically alters the frequency distribution of the waking electroencephalogram (EEG) as an indicator of alertness corresponding to cognitive performance (7). However, large interindividual differences exist in the degree of cognitive performance decline during sleep deprivation (3). In a trait-like process, some individuals keep high-level performance during sustained wakefulness, whereas others suffer from severe performance loss (3). The neuro-molecular mechanisms in the brain responsible for these different vulnerabilities are still largely unknown. Caffeine, commonly consumed for fighting fatigue, promotes wakefulness via adenosine receptor antagonism. It seems likely that the adenosinergic system is a neurochemical link between performance and sleep (8). Adenosine is contributing to the homeostatic process of sleep-wake regulation (for review, see refs. 9-12). As has been shown in cats and rats, extracellular adenosine concentration fluctuates rhythmically in many brain regions, such as the basal forebrain, increasing during wakefulness and decreasing during sleep: it thereby induces sleep after wake extension and is in turn restored to baseline levels after recovery sleep (13). For additional information on adenosine, see...

show abstract

Section: Discussionmentioning

confidence: 99%

“…It has been proposed that the development of depressive symptoms is associated with a dysfunction in this homeostatic sleep drive (15). Recently a synaptic plasticity model of therapeutic sleep deprivation in major depression has been proposed (16).…”

mentioning

confidence: 99%

Recovery sleep after extended wakefulness restores elevated A ₁ adenosine receptor availability in the human brain

Elmenhorst

Hennecke

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…In contrast to NH mice, the H line exhibited no change in SWA, indicating an impairment of the homeostatic regulation of sleep in these mice, just like in depressed patients (Armitage et al, 2000;Borbely, 1987). Recombinant offsprings of H and NH mice might represent an interesting paradigm to investigate the genetic control of such a deficit in sleep homeostasis (Franken et al, 2001).…”

Section: Effect Of Sleep Deprivationmentioning

confidence: 99%

“…On the other hand, it has been shown that stress-elicited activation of the hypothalamo-pituitary-adrenocortical (HPA) axis triggers a REM sleep rebound (Boutrel et al, 2002;Lena et al, 2004;Rampin et al, 1991). In depressed patients, both sleep homeostasis (Armitage et al, 2000;Borbely, 1987) and HPA axis activity (Barden et al, 1995) are frequently altered. Accordingly, the effects of sleep deprivation and of immobilization stress on subsequent sleep parameters were also investigated in H vs NH mice.…”

Section: Introductionmentioning

confidence: 99%

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Popa

Yacoubi²,

Vaugeois³

et al. 2005

Neuropsychopharmacol

View full text Add to dashboard Cite

In depressed patients, sleep undergoes marked alterations, especially sleep onset insomnia, sleep fragmentation, and disturbances of the Rapid Eye Movement (REM) sleep. Abnormalities of rest-activity rhythms and of hypothalamic-pituitary-adrenocortical function have also been described in these patients. In the present study, we examined the presence of such abnormalities in a recently developed line of mice (Helpless mice-H) that exhibit depression-like behaviors in validated tests, compared to the nonhelpless (NH) line derived from the same colony. Experiments were essentially carried out in females for which previous studies showed marked differences between H and NH lines. Compared to NH mice, the H line exhibited (i) lower basal locomotor activity, (ii) sleep fragmentation, shift towards lighter sleep stages, and facilitation of REM sleep reflected by increased amounts and decreased latency, (iii) larger response to the REM sleep promoting effect of muscarinic receptor stimulation (by arecoline). In contrast, H and NH mice were equally responsive to the REM sleep inhibitory effect of 5-HT 1A receptor stimulation (by 8-OH-DPAT). In addition, a deficiency in delta power enhancement after sleep deprivation was observed in the H group, and acute immobilization stress in this group failed to elicit a REM sleep rebound and was associated with a long-lasting raise in serum corticosterone levels. These results further validate H mice as a depression model and suggest they might be of particular interest for investigating the neurobiological mechanisms and possibly genetic substrates underlying sleep alterations associated with depression.

show abstract

“…It is believed that the homeostatic state is illustrated by the delta activity, whereas REM sleep and sleep duration reflect the circadian rhythm. According to the two-process model of sleep regulation by Borbély (1987Borbély ( , 1994, the propensity for sleep is a combination of Process-S and Process-C. Process-S refers to a homeostatic function. Process-C refers to sleep-independent, circadian processes.…”

Section: Homeostatic Function and Biological Rhythmsmentioning

confidence: 99%

Sleep, psychological symptoms and quality of life in patients undergoing coronary artery bypass grafting

Edéll-Gustafsson

1999

Nordic Journal of Psychiatry

View full text Add to dashboard Cite

In this thesis sleep, psychological symptoms and quality of life (Qol) in patients undergoing coronary artery bypass grafting (CABG) at the University Hospital in Linköping were evaluated. Interviews and 24-hour polysomnography were performed prior to surgery, immediately after surgery and again at one month, with a six-monthfollow-up mailed questionnaire. Habitual sleep was evaluated using the Uppsala Sleep Inventory questionnaire and a diary the recorded mornings. The Spielberger State of Anxiety Scale and the Zung´s Self-rating Depression Scale were used to measure anxiety and depression, respectively. Physical functional capacity was assessed according to the New York Heart Association´s (NYHA) classes and Qol, with the Nottingham Health Profile instrument (NHP).A retrospective evaluation of nurse's documentation about sleep was also performed. In addition, the quality and quantity of sleep were assessed before surgery and in the immediate postoperative period in a pilot study, with a one-month follow-up interview. The results indicated disturbed sleep, and changes in behaviour and mental state after surgery due to fragmented sleep, pain and anxiety.Forty-four patients were examined prior to surgery. The results showed that almost two-fifths experienced too little sleep habitually and 50 % had a combination of at least two sleep problems. Poorer health, higher level of anxiety and increased difficulties maintaining sleep (DMS) were consistent with significantly longer sleep latency, increased fragmented sleep, and reduced stages 3 and 4 and REM sleep measured by polysomnography. The level of Qol on the NHP was significantly associated with objectively measured sleep.In the immediate period following CABG there is a changed distribution of sleep, with a reduction of nocturnal sleep duration and an increase in daytime sleep, which had almost returned to preoperative values one month after surgery. Qol was significantly improved six months after surgery compared to before surgery.It was noted that patients with a more anxiety prone reactivity during six months following CABG had significantly more sleep disturbances, reduced energy and functional physical capacity, and lower quality of life, compared to those without such reactivity. Significantly more sleep disturbances, reduced energy and lower quality of life were more prominent among those with sadness/depression or cognitive/behavioural fatigue as reactions to sleep loss. A higher degree of cognitive/behavioural fatigue and dysphoria reactions were associated with a higher NYHA class.In conclusion, patients with coronary artery disease have poor quantity and quality of sleep. Increased psychological symptoms in patients with CAD prior to surgery were associated with greater symptoms six months after surgery. Physical functional capacity and quality of life were significantly improved six months after surgery

show abstract

The S-Deficiency Hypothesis of Depression and the Two-process Model of Sleep Regulation

Cited by 157 publications

References 11 publications

Recovery sleep after extended wakefulness restores elevated A ₁ adenosine receptor availability in the human brain

Recovery sleep after extended wakefulness restores elevated A ₁ adenosine receptor availability in the human brain

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Sleep, psychological symptoms and quality of life in patients undergoing coronary artery bypass grafting

Contact Info

Product

Resources

About

The S-Deficiency Hypothesis of Depression and the Two-process Model of Sleep Regulation

Cited by 157 publications

References 11 publications

Recovery sleep after extended wakefulness restores elevated A 1 adenosine receptor availability in the human brain

Recovery sleep after extended wakefulness restores elevated A 1 adenosine receptor availability in the human brain

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Sleep, psychological symptoms and quality of life in patients undergoing coronary artery bypass grafting

Contact Info

Product

Resources

About

Recovery sleep after extended wakefulness restores elevated A ₁ adenosine receptor availability in the human brain

Recovery sleep after extended wakefulness restores elevated A ₁ adenosine receptor availability in the human brain