Stress induced cognitive deficit is differentially modulated in BALB/c and C57Bl/6 mice

Palumbo, María Laura; Canzobre, Mariela C; Pascuan, Cecilia; Rı́os, Hugo; Wald, Miriam; Genaro, Ana Marı́a

doi:10.1016/j.jneuroim.2009.11.005

Cited by 59 publications

(50 citation statements)

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“…The stress protocol was slightly modified from those used in previous reports (34,38). Briefly, there was one 16-h period of water deprivation; two periods of continuous overnight illumination; two periods (7 and 17 h) of 45°cage tilt; one 17-h period in a cage without bedding chips; one period (8 h) of food deprivation; and one 17-h period of paired housing.…”

Section: Methodsmentioning

confidence: 99%

“…First, to examine the influence of chronic stress on circadian clock gene expressions in the liver, BALB/c mice were divided into two groups: one was housed under ordinary conditions (Control-BALB) and the other was subjected to CMS (CMS-BALB) (34,38,39,53). Serum parameters and hepatic gene expressions were analyzed 1 day after the last day of CMS (Fig.…”

Section: Cms Alters Circadian Mrna Expression Profiles Of Core Clock mentioning

confidence: 99%

“…CHRONIC STRESS PERTURBS HEPATIC CLOCK sterone levels (38). Therefore, we examined the effects of CMS on hepatic core clock gene expressions in C57BL/6 mice.…”

Section: E303mentioning

confidence: 99%

“…Stress is defined as any situation capable of perturbing physiological or psychological homeostasis (38). Health disorders that are associated with dysfunction of the stress system are now major problems in western societies (9).…”

mentioning

confidence: 99%

“…Therefore, we hypothesized that chronic stress affects the circadian rhythm of core clock gene expressions in the liver via the HPA axis, followed by alterations in metabolism-related genes. The chronic mild stress (CMS) procedure is widely used for analyzing stress effects in experimental animal models (34,38,39,53). To test our hypothesis, we examined the influences of CMS on circadian clock gene expressions in the liver.…”

mentioning

confidence: 99%

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Chronic mild stress alters circadian expressions of molecular clock genes in the liver

Takahashi

Yamada

Tsukita

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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Chronic stress is well known to affect metabolic regulation. However, molecular mechanisms interconnecting stress response systems and metabolic regulations have yet to be elucidated. Various physiological processes, including glucose/ lipid metabolism, are regulated by the circadian clock, and core clock gene dysregulation reportedly leads to metabolic disorders. Glucocorticoids, acting as end-effectors of the hypothalamus-pituitary-adrenal (HPA) axis, entrain the circadian rhythms of peripheral organs, including the liver, by phase-shifting core clock gene expressions. Therefore, we examined whether chronic stress affects circadian expressions of core clock genes and metabolism-related genes in the liver using the chronic mild stress (CMS) procedure. In BALB/c mice, CMS elevated and phase-shifted serum corticosterone levels, indicating overactivation of the HPA axis. The rhythmic expressions of core clock genes, e.g., Clock, Npas2, Bmal1, Per1, and Cry1, were altered in the liver while being completely preserved in the hypothalamic suprachiasmatic nuculeus (SCN), suggesting that the SCN is not involved in alterations in hepatic core clock gene expressions. In addition, circadian patterns of glucose and lipid metabolism-related genes, e.g., peroxisome proliferator activated receptor (Ppar) ␣, Ppar␥-1, Ppar␥-coactivator-1␣, and phosphoenolepyruvate carboxykinase, were also disturbed by CMS. In contrast, in C57BL/6 mice, the same CMS procedure altered neither serum corticosterone levels nor rhythmic expressions of hepatic core clock genes and metabolismrelated genes. Thus, chronic stress can interfere with the circadian expressions of both core clock genes and metabolism-related genes in the liver possibly involving HPA axis overactivation. This mechanism might contribute to metabolic disorders in stressful modern societies. stress; liver clock; metabolic disorders; hypothalamus-pituitary-adrenal axis VARIOUS BEHAVIORAL AND PHYSIOLOGICAL processes, including feeding behavior and energy metabolism, exhibit circadian (i.e., 24-h) rhythmicity, which may play a role in maintaining functional homeostasis. These rhythms are regulated by the circadian clock system, which is composed of transcriptional/ translational feedback loops. Although the mammalian master pacemaker is located in the hypothalamic suprachiasmatic nucleus (SCN), the core clock machinery has been identified in almost all peripheral tissues, including the liver (41). In brief, each cell contains a set of core clock genes, such as Clock, Bmal1, Cry 1-2, Per 1-3, and nuclear receptors (Rev-erb␣, ROR). The CLOCK/BMAL1 heterodimer regulates the production of proteins such as PERs and CRYs, which in turn regulate the production of BMAL1 (44). Through these feedback loops, the expressions of core clock genes generate endogenous rhythms of numerous protein expressions, leading to rhythmic functioning of cells and tissues over an ϳ24-h period (12). The molecular clock has been demonstrated to modulate energy metabolism by controlling the expressions and activi...

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Section: Methodsmentioning

confidence: 99%

Section: Cms Alters Circadian Mrna Expression Profiles Of Core Clock mentioning

confidence: 99%

“…CHRONIC STRESS PERTURBS HEPATIC CLOCK sterone levels (38). Therefore, we examined the effects of CMS on hepatic core clock gene expressions in C57BL/6 mice.…”

Section: E303mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Chronic mild stress alters circadian expressions of molecular clock genes in the liver

Takahashi

Yamada

Tsukita

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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Molecular links between endocrine, nervous and immune system during chronic stress

2020

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Introduction The stress response is different in various individuals, however, the mechanisms that could explain these distinct effects are not well known and the molecular correlates have been considered one at the time. Particular harmful conditions occur if the subject, instead to cope the stressful events, succumb to them, in this case, a cascade reaction happens that through different signaling causes a specific reaction named “sickness behaviour.” The aim of this article is to review the complex relations among important molecules belonging to Central nervous system (CNS), immune system (IS), and endocrine system (ES) during the chronic stress response. Methods After having verified the state of art concerning the function of cortisol, norepinephrine (NE), interleukin (IL)‐1β and melatonin, we describe as they work together. Results We propose a speculative hypothesis concerning the complex interplay of these signaling molecules during chronic stress, highlighting the role of IL‐1β as main biomarker of this effects, indeed, during chronic stress its increment transforms this inflammatory signal into a nervous signal (NE), in turn, this uses the ES (melatonin and cortisol) to counterbalance again IL‐1β. During cortisol resistance, a vicious loop occurs that increments all mediators, unbalancing IS, ES, and CNS networks. This IL‐1β increase would occur above all when the individual succumbs to stressful events, showing the Sickness Behaviour Symptoms. IL‐1β might, through melatonin and vice versa, determine sleep disorders too. Conclusion The molecular links here outlined could explain how stress plays a role in etiopathogenesis of several diseases through this complex interplay.

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Chronic exposure to stress predisposes to higher autoimmune susceptibility in C57BL/6 mice: Glucocorticoids as a double‐edged sword

et al. 2013

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Stress activates the hypothalamic-pituitary-adrenocortical axis to promote the release of corticosterone (CORT), which consequently suppresses pathogenic stimulation of the immune system. Paradoxically, however, stress often promotes autoimmunity through yet unknown mechanisms. Here we investigated how chronic variable stress (CVS), and the associated alterations in CORT levels, affect the susceptibility to experimental autoimmune encephalomyelitis (EAE) in female and male C57BL/6 mice. Under baseline (nonstressed) conditions, females exhibited substantially higher CORT levels and an attenuated EAE with less mortality than males. However, CVS induced a significantly worsened EAE in females, which was prevented if CORT signaling was blocked. In addition, females under CVS conditions showed a shift toward proinflammatory Th1/Th17 versus Th2 responses and a decreased proportion of CD4 + CD25 + Treg cells. This demonstrates that whereas C57BL/6 female mice generally exhibit higher CORT levels and an attenuated form of EAE than males, they become less responsive to the immunosuppressive effects of CORT under chronic stress and thereby prone to a higher risk of destructive autoimmunity.Keywords: CD4 T cells r Chronic stress r Corticosterone r EAE Additional supporting information may be found in the online version of this article at the publisher's web-site IntroductionIt has been well established that stress may substantially affect the homeostatic regulation of the immune system [1][2][3]. In most Correspondence: Dr. Alon Monsonego e-mail: alonmon@bgu.ac.il animal models studied thus far, stressful triggers such as fear, maternal deprivation, social threat, or physiological challenge have been shown to induce immunosuppression associated with increased susceptibility to allergies and infectious diseases [1,4,5]. These effects are mediated by the hypothalamic-pituitary-adrenal (HPA) axis, a complex network linking the nervous, endocrine and immune systems [6,7].The HPA axis can be triggered by stress or by proinflammatory cytokines (e.g. IL-1, IL-6, and TNF-α) to ultimately result in C 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu Eur. J. Immunol. 2013. 43: 758-769 Immunomodulation 759 the secretion of corticosterone (CORT) from the adrenal glands to the circulation [8]. CORT, in turn, acts to suppress the activation, proliferation, and trafficking of immune cells [9,10] and plays a role in autoimmune regulation via shifting from Th1/Th17 pro-inflammatory to Th2 antiinflammatory responses [11][12][13]. Indeed, previous studies have shown that rats producing lower CORT levels (e.g. due to genetic manipulation or adrenalectomy) are more susceptible to pathogenic autoimmunity [14]. CORT is therefore often used as an immunosuppressor in the clinical treatment of inflammatory and autoimmune diseases [9,15,16]. Regardless of the immunosuppressive effects of CORT, chronic exposure to stress has also been linked with relapse of autoimmune diseases such as multiple sclerosis [17,18] and psoriasis [19,2...

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Stress induced cognitive deficit is differentially modulated in BALB/c and C57Bl/6 mice

Cited by 59 publications

References 49 publications

Chronic mild stress alters circadian expressions of molecular clock genes in the liver

Chronic mild stress alters circadian expressions of molecular clock genes in the liver

Molecular links between endocrine, nervous and immune system during chronic stress

Chronic exposure to stress predisposes to higher autoimmune susceptibility in C57BL/6 mice: Glucocorticoids as a double‐edged sword

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