Effect of chronic mild stress on circadian rhythms in the locomotor activity in rats

Górka, Z; Moryl, E; Papp, Mariusz

doi:10.1016/0091-3057(95)02173-6

Cited by 97 publications

(61 citation statements)

References 25 publications

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“…SDD, but not SDL, mice showed a significant decrease in dark phase activity on days 7, 14, and 20 when compared with SHC mice. At least for the SDD group, our data are consistent with a previous study, reporting a decrease in activity during the active, but not inactive, phase after chronic mild stress in rats (Gorka et al 1996). Given that SDD mice were predictably exposed to SD for 19 consecutive days (except observation days) at the beginning of the dark phase, a reduction in dark phase activity is likely to indicate that SDD mice are expecting the next SD.…”

Section: Discussionsupporting

confidence: 81%

“…In line with this, it was recently shown in rodents that chronic unpredictable stress affects suprachiasmatic nucleus (SCN) functionality, the central pacemaker of the circadian system in mammals, by dampening the amplitude of circadian PERIOD2 (PER2) protein expression, one of the main clock proteins involved in internal rhythm generation (Jiang et al 2011). In addition, various biological diurnal rhythms generated and fine-tuned by the SCN such as locomotor activity (Gorka et al 1996), body temperature (Ushijima et al 2006), heart rate (Grippo et al 2003), sleep (Moreau et al 1995), and plasma glucocorticoid (GC) levels (Ottenweller et al 1994) are also affected by repeated exposure to non-psychosocial stressors.…”

Section: Introductionmentioning

confidence: 87%

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Time matters: pathological effects of repeated psychosocial stress during the active, but not inactive, phase of male mice

Bartlang¹,

Neumann²,

Slattery³

et al. 2012

Journal of Endocrinology

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Recent findings in rats indicated that the physiological consequences of repeated restraint stress are dependent on the time of day of stressor exposure. To investigate whether this is also true for clinically more relevant psychosocial stressors and whether repeated stressor exposure during the light phase or dark phase is more detrimental for an organism, we exposed male C57BL/6 mice to social defeat (SD) across 19 days either in the light phase between Zeitgeber time (ZT)1 and ZT3 (SDL mice) or in the dark phase between ZT13 and ZT15 (SDD mice). While SDL mice showed a prolonged increase in adrenal weight and an attenuated adrenal responsiveness to ACTH in vitro after stressor termination, SDD mice showed reduced dark phase home-cage activity on observation days 7, 14, and 20, flattening of the diurnal corticosterone rhythm, lack of social preference, and higher in vitro IFNg secretion from mesenteric lymph node cells on day 20/21. Furthermore, the colitis-aggravating effect of SD was more pronounced in SDD than SDL mice following dextran sulfate sodium treatment. In conclusion, the present findings demonstrate that repeated SD effects on behavior, physiology, and immunology strongly depend on the time of day of stressor exposure. Whereas physiological parameters were more affected by SD during the light/inactive phase of mice, behavioral and immunological parameters were more affected by SD during the dark phase. Our results imply that repeated daily SD exposure has a more negative outcome when applied during the dark/active phase. By contrast, the minor physiological changes seen in SDL mice might represent beneficial adaptations preventing the formation of those maladaptive consequences.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 87%

Time matters: pathological effects of repeated psychosocial stress during the active, but not inactive, phase of male mice

Bartlang¹,

Neumann²,

Slattery³

et al. 2012

Journal of Endocrinology

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“…The CMS model appears to be particularly appropriate for studying antidepressant-like activity of compounds with chronobiotic properties since, apart from a deficit in their responsiveness to reward, animals exposed to the CMS procedure show advanced phase shift of diurnal rhythms (Gorka et al, 1996), diurnal variation with symptoms worst at the start of the dark (ie active) phase (D'Aquila et al, 1997), and a variety of sleep disorders characteristic of depression, including decreased rapid eye movement (REM) sleep latency, increased number of REM sleep episodes, and more fragmented sleep patterns (Moreau et al, 1995;Cheeta et al, 1997). All these findings indicate that the CMS procedure causes a generalized disorganization of internal rhythms, which are postulated to play an important role in the pathophysiology of depression (Wehr and Wirz-Justice, 1982).…”

Section: Introductionmentioning

confidence: 99%

Effect of Agomelatine in the Chronic Mild Stress Model of Depression in the Rat

Papp

Gruca

Boyer

et al. 2002

Neuropsychopharmacol

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242

166

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Chronic mild stress (CMS), a well-validated model of depression, was used to study the effects of the melatonin agonist and selective 5-HT 2C antagonist agomelatine (S 20098) in comparison with melatonin, imipramine, and fluoxetine. All drugs were administered either 2 h before (evening treatment) or 2 h after (morning treatment) the dark phase of the 12-h light/dark cycle. Chronic (5 weeks) evening treatment with agomelatine or melatonin (both at 10 and 50 mg/kg i.p.) dose-dependently reversed the CMS-induced reduction in sucrose consumption. The magnitude and time course of the action of both drugs was comparable to that of imipramine and fluoxetine (both at 10 mg/kg i.p.); however, melatonin was less active than agomelatine at this dose. The effect of evening administration of agomelatine and melatonin was completely inhibited by an acute injection of the MT 1 /MT 2 antagonist, S 22153 (20 mg/kg i.p.), while the antagonist had no effect in animals receiving fluoxetine or imipramine. When the drugs were administered in the morning, agomelatine caused effects similar to those observed after evening treatment (with onset of action faster than imipramine) but melatonin was ineffective. Moreover, melatonin antagonist, S 22153, did not modify the intakes in stressed animals receiving morning administration of agomelatine and in any other control and stressed groups tested in this study. These data demonstrate antidepressant-like activity of agomelatine in the rat CMS model of depression, which was independent of the time of drug administration. The efficacy of agomelatine is comparable to that of imipramine and fluoxetine, but greater than that of melatonin, which had no antidepressant-like activity after morning administration. While the evening efficacy of agomelatine can be related to its melatonin receptors agonistic properties, its morning activity, which was not inhibited by a melatonin antagonist, indicates that these receptors are certainly required, but not sufficient to sustain the agomelatine efficacy. It is therefore suggested that the antidepressant-like activity of agomelatine depends on some combination of its melatonin agonist and 5-HT 2C antagonist properties.

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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. Ce faisceau d'arguments indique que toute amélioration de la synchronisation des rythmes biologiques d'un individu dépressif pourrait avoir un effet bénéfique sur les épisodes dépressifs.…”

Section: Dépression Et Rythmes Circadiens Anormauxunclassified

“…Des modèles génomiques (délétion des sous-type de récepteurs du CRH, des tachykinines ou du transporteur de la sérotonine, antisense des récepteurs des glucocorticoïdes) et génétiques (rat Fawn Hooded, rat de la lignée Flinders Sensitive) ont été mis au point, ainsi qu'un modèle de lésion (rat ayant subi une bulbectomie). Dans le cadre du développement d'un agoniste mélatoninergique, le test de résignation acquise, le stress chronique modéré et le modèle des souris transgé-niques avec un déficit des récepteurs des glucocorticoïdes sont des modèles plus particulièrement intéressants, car des perturbations des rythmes circadiens et du sommeil ont été clairement démontrées chez ces animaux « résignés » [27] et en « anhédonie » [15]. De fait, la mélatonine est active dans le modèle de stress léger chronique chez des souris C3H/He [28] et, dans une moindre mesure, chez des rats soumis à ce test [29].…”

Section: Développement D'un Antidépresseur à Mécanisme D'action Innovunclassified

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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Effect of chronic mild stress on circadian rhythms in the locomotor activity in rats

Cited by 97 publications

References 25 publications

Time matters: pathological effects of repeated psychosocial stress during the active, but not inactive, phase of male mice

Time matters: pathological effects of repeated psychosocial stress during the active, but not inactive, phase of male mice

Effect of Agomelatine in the Chronic Mild Stress Model of Depression in the Rat

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

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