Circadian rhythms in depression and recovery: Evidence for blunted amplitude as the main chronobiological abnormality

Souêtre, E.; Salvati, E.; Belugou, J.L.; Pringuey, D.; Candito, M.; Krebs, B; Ardisson, J L; Darcourt, G

doi:10.1016/0165-1781(89)90207-2

Cited by 355 publications

(180 citation statements)

References 44 publications

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“…In addition, the amplitude of locomotor activity rhythm was smaller in H mice. These results are similar to those a b reported for other animal models of depression (Overstreet, 1993;Solberg et al, 2001) and are reminiscent of the behavioural inhibition and the global flattening of circadian rhythms observed in depressed patients (Bunney and Bunney, 2000;Souetre et al, 1989). In NH mice, the changes in core temperature across the 24 h period were directly correlated with those of locomotor activity (Bunney and Bunney, 2000).…”

Section: Locomotor Activity and Sleep-wakefulness Cycles Under Baselisupporting

confidence: 89%

“…It is associated with characteristic sleep impairments, notably difficulties in falling asleep, reduction of the rapid eye movement (REM) sleep latency, sleep fragmentation, and early morning awakenings (Adrien, 2002;Benca, 2000). In addition, abnormalities of circadian rhythms, affecting notably nycthemeral variations in rest-activity, and body temperature, have been described in depressed patients (Avery et al, 1999;Bunney and Bunney, 2000;Souetre et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

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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

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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.

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Section: Locomotor Activity and Sleep-wakefulness Cycles Under Baselisupporting

confidence: 89%

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

show abstract

“…Indeed, blunted or abnormal circadian rhythms in a variety of bodily functions including body temperature, plasma cortisol, norepinephrine, thyroid stimulating hormone, blood pressure, pulse, and melatonin have been found in depressed and bipolar patients (Atkinson et al, 1975;Kripke et al, 1978;Souetre et al, 1989). Interestingly, these rhythms seem to return to normal with antidepressant or mood stabilizer treatment and patient recovery.…”

Section: A Generally Disrupted Clockmentioning

confidence: 99%

Circadian genes, rhythms and the biology of mood disorders

McClung

2007

Pharmacology & Therapeutics

585

386

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For many years, researchers have suggested that abnormalities in circadian rhythms may underlie the development of mood disorders such as bipolar disorder, major depression and seasonal affective disorder. Furthermore, some of the treatments that are currently employed to treat mood disorders are thought to act by shifting or "resetting" the circadian clock, including total sleep deprivation and bright light therapy. There is also reason to suspect that many of the mood stabilizers and antidepressants used to treat these disorders may derive at least some of their therapeutic efficacy by affecting the circadian clock. Recent genetic, molecular and behavioral studies implicate individual genes that make up the clock in mood regulation. As well, important functions of these genes in brain regions and neurotransmitter systems associated with mood regulation is becoming apparent. In this review, the evidence linking circadian rhythms and mood disorders, and what is known about the underlying biology of this association, is presented.

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“…La désorganisation des rythmes circadiens, tels que le rythme veille/sommeil ou les rythmes hormonaux [12,13], est caractéristique d'un grand nombre de troubles de l'humeur, y compris de la dépression, et suscite un intérêt croissant. Une désorganisation des rythmes circadiens a été mise en évidence dans des modèles animaux de dépression [14,15], et il est connu qu'une désynchronisation des rythmes circadiens chez l'homme peut déclencher des épi-sodes dépressifs.…”

Section: Dépression Et Rythmes Circadiens Anormauxunclassified

Comment déveloper un antidépresseur au mécanisme d’action innovant : l’exemple de l’agomélatine

Mocaër

Delalleau

et al. 2005

Med Sci (Paris)

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Les travaux les plus récents ont confirmé la forte pré-valence de la dépression : sur leur vie entière, 20 % des femmes et 10 % des hommes ont fait, font ou feront un épisode dépressif. De tels chiffres sont à l'évidence marquants ; ils le sont encore plus lorsqu'on s'intéresse à la complication majeure de la dépression, le suicide, qui se chiffre à 12 000 décès par an dans des pays comme la France. D'une manière générale, on estime que 15 % des patients déprimés décè-dent par suicide [1]. À la souffrance personnelle et familiale que représente la dépression s'ajoute le poids social important de cette pathologie : la dépression représente d'ores et déjà l'une des premières causes d'arrêts de travail dans les pays occidentaux. Malgré l'arsenal thérapeutique mis à la disposition du corps médical, en particulier SSRI (selective serotonin reuptake inhibitors) et SNRI (serotonin norepinephrine reuptake inhibitors), 30 % de la population dépressive n'est pas traitée. Les SSRI sont relativement bien tolérés comparativement aux antidépresseurs imipraminiques, mais présentent un certain nombre d'effets indésirables tels que des effets gastro-intestinaux et des perturbations de la fonction sexuelle ou du sommeil [2]. Un syndrome de sevrage à l'arrêt du traitement a également été rapporté avec l'emploi de certains SSRI [3]. Il existe donc un besoin évident de nouveaux traitements, plus efficaces, mieux tolérés et d'action plus rapide.

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Circadian rhythms in depression and recovery: Evidence for blunted amplitude as the main chronobiological abnormality

Cited by 355 publications

References 44 publications

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

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

Circadian genes, rhythms and the biology of mood disorders

Comment déveloper un antidépresseur au mécanisme d’action innovant : l’exemple de l’agomélatine

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