Corticotropin-releasing hormone mRNA levels in response to chronic mild stress rise in male but not in female rats while tyrosine hydroxylase mRNA levels decrease in both sexes

Dunčko, Roman; Kiss, Alexander; Škultétyová, Ivana; Rusnak, Milan; Ježová, Daniela

doi:10.1016/s0306-4530(00)00040-8

Cited by 177 publications

(120 citation statements)

References 25 publications

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“…Indeed, our data are consistent with the previous findings that rats exposed to stressors consume less sucrose than the controls [13,18,24,26] . This indicates that anhedonia, the core symptom of depression, can be induced by CUMS in rats.…”

supporting

confidence: 93%

“…Chronic mild stress leads to an increase in the activity of the hypothalamic-pituitary-adrenal (HPA) axis, including adrenal hypertrophy and corticosterone hypersecretion [11,12] , and alters CRH mRNA level in the PVN [13] . In addition to the PVN of hypothalamus, the amygdala also mediates neuroendocrine, autonomic, and behavioral changes during stress [14,15] .…”

Section: Introductionmentioning

confidence: 99%

“…The present study aimed to investigate CRH expression level in PVN and in the amygdala in rats with CUMS, a model of depression. [13,18,19] . The animals were randomly exposed to one of the following stressors each day: hot stress in the oven at 45 °C for 5 min, swimming in 8 °C water for 5 min, shaking frequently (100/ min) for 5 min, 60 inescapable electric foot shocks at a 1.5 mA intensity and 2 s duration with 1 s intervals, tail clamping for 1 min, water and food deprivation for 24 h, and placement in cages that were tilted 30 ° from the horizontal.…”

Section: Introductionmentioning

confidence: 99%

“…It has been revealed that CRH mRNA level is increased in PVN after chronic mild stress [13] . Our finding is consistent with the previous reports that demonstrate hyperactivation of CRH neurons in PVN both in stressed rats [13] and in the brain of depressive patients [3,4] . Besides, we have found in the same model that CRH mRNA expression is increased after CUMS [27] .…”

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confidence: 99%

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Increased expression level of corticotropin-releasing hormone in the amygdala and in the hypothalamus in rats exposed to chronic unpredictable mild stress

et al. 2010

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Objective Corticotropin-releasing hormone (CRH) plays an important role in neuroendocrine, autonomic and behavioral responses to stressors. In the present study, the effect of chronic unpredictable mild stress (CUMS) on CRH neurons was investigated in rat brain. Methods The rats were exposed to one of the stressors each day for 21 d. Immunostaining was performed to detect the CRH-positive neurons in the paraventricular nucleus (PVN) of the hypothalamus and in amygdala.Results After the stress protocol, the animals showed a reduction in body weight gain as well as reduced sucrose preference and locomotor activity. Interestingly, the CRH neurons in both PVN and central nucleus of the amygdala (CeA) were stimulated by CUMS. The densities of CRH-containing neurons in both PVN and CeA were significantly higher than those in control group. Conclusion The CRH systems in PVN and CeA may both contribute to depression-like behaviors during CUMS.

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supporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Increased expression level of corticotropin-releasing hormone in the amygdala and in the hypothalamus in rats exposed to chronic unpredictable mild stress

et al. 2010

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“…Among the negative consequences of chronic stress exposure are changes in brain plasticity, with consequent development of psychopathologies and cognitive impairments (Duncko et al 2001, Hemmerle et al 2012, Izakova & Jezova 2013. Stress-induced decreases in parameters of brain plasticity, such as glutamatergic neurotransmission, long-term potentiation, synaptogenesis, and adult neurogenesis, are under the influence of several regulatory factors including posterior pituitary neuropeptides (McEwen 2012).…”

Section: Introductionmentioning

confidence: 99%

Effects of atosiban on stress-related neuroendocrine factors

Babic¹,

Pokusa²,

Danevova³

et al. 2015

Journal of Endocrinology

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Atosiban, an oxytocin/vasopressin receptor antagonist, is used to decrease preterm uterine activity. The risk of preterm delivery is undoubtedly associated with stress, but potential side effects of atosiban on neuroendocrine functions and stress-related pathways are mostly unknown. These studies were designed to test the hypothesis that the chronic treatment of rats with atosiban modulates neuroendocrine functions under stress conditions. Male rats were treated (osmotic minipumps) with atosiban (600 mg/kg per day) or vehicle and were restrained for 120 min/day for 14 days. All animals were treated with a marker of cell proliferation 5-bromo-2-deoxyuridine. Anxiety-like behavior was measured using an elevated plus-maze. Treatment with atosiban failed to modify plasma concentrations of the stress hormones ACTH and corticosterone, but led to a rise in circulating copeptin. Atosiban increased prolactin levels in the non-stressed group. Oxytocin receptor mRNA levels were increased in rats exposed to stress. Treatment with atosiban, in both control and stressed animals, resulted in a decrease in oxytocin receptor gene expression in the hypothalamus. No changes were observed in vasopressin receptor 1A and 1B gene expression. The decrease in hippocampal cell proliferation induced by stress exposure was not modified by atosiban treatment. This study provides the first data, to our knowledge, revealing the effect of atosiban on gene expression of oxytocin receptors in the brain. Atosiban-induced enhancement of plasma copeptin indicates an elevation in vasopressinergic tone with potential influence on water-electrolyte balance.

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Sex differences in hypothalamic–pituitary–adrenal axis regulation after chronic unpredictable stress

2020

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Introduction: Exposure to stress, mediated through the hypothalamic-pituitary-adrenal (HPA) axis, elicits sex differences in endocrine, neurological, and behavioral responses. However, the sex-specific factors that confer resilience or vulnerability to stress and stress-associated psychiatric disorders remain largely unknown. The evident sex differences in stress-related disease prevalence suggest the underlying differences in the neurobiological underpinnings of HPA axis regulation. Method:Here, we used a chronic unpredictable stress (CUS) model to investigate the behavioral and biochemical responses of the HPA axis in C57BL/6 mice. Animals were tested in the open field and forced swim test to examine anxiety-like and depressivelike behaviors. Plasma corticosterone levels were measured after behavior and CUS, and glucocorticoid receptor (GR) expression and cytosolic and nuclear fractions of binding protein FKBP51 expression were taken to measure function and regulation of the stress response. Results:Our results indicate increased depressive-like behavior in males and females which correlated with increased corticosterone levels following CUS. However, females displayed more anxiety-like behaviors with and without CUS. Interestingly, we found trends toward dysregulation of GR protein expression in CUS females, and an increase in the GR inhibitory protein, FKBP51, in the cytosol of CUS males but not females. Conclusion:These results suggest biochemical alterations to the HPA axis regulation which may elicit a glucocorticoid resistance in females after chronic stress and may contribute to the sex-biased vulnerability to stress-related psychiatric disorders. K E Y W O R D Schronic stress, FKBP51, glucocorticoid receptor, HPA axis, sex differences

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Corticotropin-releasing hormone mRNA levels in response to chronic mild stress rise in male but not in female rats while tyrosine hydroxylase mRNA levels decrease in both sexes

Cited by 177 publications

References 25 publications

Increased expression level of corticotropin-releasing hormone in the amygdala and in the hypothalamus in rats exposed to chronic unpredictable mild stress

Increased expression level of corticotropin-releasing hormone in the amygdala and in the hypothalamus in rats exposed to chronic unpredictable mild stress

Effects of atosiban on stress-related neuroendocrine factors

Sex differences in hypothalamic–pituitary–adrenal axis regulation after chronic unpredictable stress

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