“…This was not the case for H mice that exhibited decreased wakefulness. In the same manner, we found no abnormality of delta power during deep SWS in H mice, whereas this is a constant feature of depression, especially in women (Armitage et al, 2000). However, depressed patients suffer also decreased sleep continuity, difficulties falling asleep and maintaining sleep, and early morning awakenings.…”
“…Globally, the present model mimics these characteristics, illustrated by sleep fragmentation and the frequent awakenings. In addition, deficits in locomotor activity, REM sleep alterations, and sleep homeostasis deficiency also evoke the impairments found in depressed patients (Armitage et al, 2000;Lustberg and Reynolds, 2000).…”
“…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.…”
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.
“…This was not the case for H mice that exhibited decreased wakefulness. In the same manner, we found no abnormality of delta power during deep SWS in H mice, whereas this is a constant feature of depression, especially in women (Armitage et al, 2000). However, depressed patients suffer also decreased sleep continuity, difficulties falling asleep and maintaining sleep, and early morning awakenings.…”
“…Globally, the present model mimics these characteristics, illustrated by sleep fragmentation and the frequent awakenings. In addition, deficits in locomotor activity, REM sleep alterations, and sleep homeostasis deficiency also evoke the impairments found in depressed patients (Armitage et al, 2000;Lustberg and Reynolds, 2000).…”
“…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.…”
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.
“…Adults with depression also show evidence of sleep EEG dysregulation with a breakdown in the degree of synchronization between ultradian (90 min) sleep EEG rhythms (i.e., low temporal coherence) (Armitage 1995;Armitage et al 1992Armitage et al , 1993Armitage et al , 1999. Low temporal coherence is more strongly a characteristic of depressed women, whereas depressed men are more likely to show reduced slow-wave or delta activity, particularly in the first Non REM (NREM) sleep period Hoffman 1997, 2001;Armitage et al 1999Armitage et al , 2000a. Such findings provide preliminary evidence that the nature of the sleep EEG abnormality in depression is gender dependent.…”
It is well known that insomnia is more frequent in women than in men throughout all age groups. In this respect insomnia resembles other psychiatric disorders that occur more frequently in women such as anxiety and depressive disorders. Since insomnia is frequently a symptom of anxiety and depression, it remains an open question whether the comorbidity with psychiatric disorders fully explains the gender differences in the prevalence of insomnia or whether gender influences sleep independently from psychiatric conditions. We analyzed sleep measures of patients diagnosed with a primary insomnia (n=86) and of an age- and sex-matched healthy control group (n=86) by polysomnography; additionally, subjective rating scales were available for 70 patients and 54 controls matched for mean age and sex ratio. Surprisingly, none of the sleep continuity measures (sleep duration, sleep efficiency, arousal index, and wake%), nor slow wave or REM sleep % showed significant gender differences in both insomniacs and healthy controls. Also, subjective estimates of sleep quality were comparable in both sexes. As expected, insomniacs strongly differed from the control group in all subjective measures of sleep. Polysomnography showed significantly reduced sleep duration and efficiency, increased arousal index, and slightly, but significantly, less REM sleep in the insomniacs as compared to the healthy controls. These studies indicate that gender seems to have, if any, relatively little influence on sleep per se. We hypothesize that the clear gender differences in the prevalence of insomnia are caused predominantly by gender differences in the prevalence of anxiety and depression. Primary insomnia may be, at least in a part of the cases, a subclinical or subthreshold form of anxiety or depression.
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