Chronic corticosterone-induced depression mediates premature aging in rats

Xie, Xiaoxian; Shen, Qichen; Ma, Lingyan; Chen, Yangyang; Zhao, Binggong; Fu, Zhengwei

doi:10.1016/j.jad.2017.12.073

Cited by 34 publications

(21 citation statements)

References 69 publications

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“…To simulate the HPA dysregulation seen in the genetic and stress-based models of depression, researchers have used exogeneous corticosterone administration in rodents (160). Robust and highly reproducible anxiety-and depression-like behaviors have been reported following chronic oral administration of corticosterone, which may or may not lead to an elevation in the level of serum corticosterone (133,(161)(162)(163)(164)(165)(166)(167)(168)(169). In addition to the behavioral changes, chronic exogeneous corticosterone is associated with several neurobiological changes seen in MDD models including the disruption of adult hippocampal neurogenesis (170), and decreased hippocampal brain derived neurotrophic factor (BDNF) (171).…”

Section: Modelling Depression Using Exogeneous Corticosterone Adminismentioning

confidence: 99%

Cortisol and Major Depressive Disorder—Translating Findings From Humans to Animal Models and Back

Nandam¹,

Brazel²,

Zhou³

et al. 2020

Front. Psychiatry

172

103

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Major depressive disorder (MDD) is a global problem for which current pharmacotherapies are not completely effective. Hypothalamic-pituitary-adrenal (HPA) axis dysfunction has long been associated with MDD; however, the value of assessing cortisol as a biological benchmark of the pathophysiology or treatment of MDD is still debated. In this review, we critically evaluate the relationship between HPA axis dysfunction and cortisol level in relation to MDD subtype, stress, gender and treatment regime, as well as in rodent models. We find that an elevated cortisol response to stress is associated with acute and severe, but not mild or atypical, forms of MDD. Furthermore, the increased incidence of MDD in females is associated with greater cortisol response variability rather than higher baseline levels of cortisol. Despite almost all current MDD treatments influencing cortisol levels, we could find no convincing relationship between cortisol level and therapeutic response in either a clinical or preclinical setting. Thus, we argue that the absolute level of cortisol is unreliable for predicting the efficacy of antidepressant treatment. We propose that future preclinical models should reliably produce exaggerated HPA axis responses to acute or chronic stress a priori, which may, or may not, alter baseline cortisol levels, while also modelling the core symptoms of MDD that can be targeted for reversal. Combining genetic and environmental risk factors in such a model, together with the interrogation of the resultant molecular, cellular, and behavioral changes, promises a new mechanistic understanding of MDD and focused therapeutic strategies.

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Section: Modelling Depression Using Exogeneous Corticosterone Adminismentioning

confidence: 99%

Cortisol and Major Depressive Disorder—Translating Findings From Humans to Animal Models and Back

Nandam¹,

Brazel²,

Zhou³

et al. 2020

Front. Psychiatry

172

103

View full text Add to dashboard Cite

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“…Stress is considered as the most common and essential factor that leads to depression, and stress paradigms have long been used to mimic critical symptoms of depression 22 . Repeated corticosterone (CORT) treatment induces depression-like behaviors that marked by significant changes in behavioral traits, neurochemistry, and brain morphology 23 , 24 . The hypothalamic–pituitary–adrenal (HPA) axis activated in response to stress in depressed patients.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of VMY-2-95 on corticosterone-induced injuries in mice and cellular models

Kong

et al. 2021

Acta Pharmaceutica Sinica B

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Nicotinic α 4 β 2 receptor antagonists have drawn increasing attention in the development of new antidepressants. In this study, we aimed to investigate the protective effect of VMY-2-95, the new selective antagonist of α 4 β 2 nicotinic acetylcholine receptor (nAChR) on corticosterone (CORT) injured mice and cellular models. Fluoxetine was applied as a positive control, and the effects of VMY-2-95 were investigated with three different doses or concentrations (1, 3, 10 mg/kg in mice, and 0.003, 0.03, 0.1 μmol/L in cells). As a result, VMY-2-95 showed significant antidepressant-like effects in the CORT injured mice by improving neuromorphic function, promoting hippocampal nerve proliferation, and regulating the contents of monoamine transmitters. Meanwhile, VMY-2-95 exhibited protective effects on cell viability, cell oxidant, cell apoptosis, and mitochondrial energy metabolism on corticosterone-impaired SH-SY5Y cells. Also, the PKA–CREB–BDNF signaling pathway was up-regulated by VMY-2-95 both in vitro and in vivo , and pathway blockers were also combined with VMY-2-95 to verify the effects furtherly. Therefore, we preliminarily proved that VMY-2-95 had protective effects in depressed mice and SH-SY5Y cells against injuries induced by corticosterone. This work indicated that the application of VMY-2-95 is a potential pharmacological solution for depression. This study also supported the development of α 4 β 2 nAChR antagonists towards neuropsychiatric dysfunctions.

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“…In adult zebra finches, telomere length in red blood cells is correlated with telomere length in the spleen, liver and brain, but not muscle or heart [74]. While avian studies in our meta-analysis used red blood cells for telomere measurement, telomere length was measured in tail muscle and liver in mammals and amphibians, which could lead to discrepancies when comparing among studies [61,[75][76].…”

Section: Discussionmentioning

confidence: 93%

“…We statistically analyzed 15 of the remaining 31 studies, the ones that provided raw data for analysis [29][30][31][32][33][34][35][36][37][38][39][40][41][42][43]. The other 16 studies appeared to fit criteria but did not provide raw data for analysis [44][45][46][47][48][49][50][51][52][53][54][55][56][57][58]. The literature and study selection process is illustrated using a PRISMA diagram (Fig 1).…”

Section: Literature Search and Study Selectionmentioning

confidence: 99%

Short-term elevations in glucocorticoids do not alter telomere lengths: A systematic review and meta-analysis of non-primate vertebrate studies

Zane

Ensminger

Vázquez‐Medina

2021

Preprint

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Background: The neuroendocrine stress response allows vertebrates to cope with stressors via the activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis, which ultimately results in the secretion of glucocorticoids (CORT). Glucocorticoids have pleiotropic effects on behavior and physiology, and might influence telomere length dynamics. During a stress event, CORT mobilizes energy towards survival mechanisms rather than to telomere maintenance. Additionally, reactive oxidative species produced in response to increased CORT levels can damage telomeres, also leading to telomere shortening. In our systematic review and meta-analysis, we tested whether CORT levels impact telomere length and if this relationship differs among time frame, life history stage, or stressor type. We hypothesized that elevated CORT levels are linked to a decrease in telomere length. Methods: To test this hypothesis, we conducted a literature search for studies investigating the relationship between telomere length and CORT levels in non-human vertebrates using four search engines Web of Science, Google Scholar, Pubmed and Scopus, last searched on September 27th, 2020. This review identified 31 studies examining the relationship between CORT and telomere length. We pooled the data using Fishers Z for 15 of these studies. All quantitative studies underwent a risk of bias assessment. This systematic review study was registered in the Open Science Framework Registry (https://osf.io/rqve6). Results: The pooled effect size from fifteen studies and 1066 study organisms shows no relationship between CORT and telomere length (Fishers Z= 0.1042, 95% CI = 0.0235; 0.1836). While these results support some previous findings, other studies have found a direct relationship between CORT and telomere dynamics, suggesting underlying mechanisms or concepts that are not currently taken into account in our analysis. The risk of bias assessment revealed an overall low risk of bias with occasional instances of bias from missing outcome data or bias in the reported result.

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Chronic corticosterone-induced depression mediates premature aging in rats

Cited by 34 publications

References 69 publications

Cortisol and Major Depressive Disorder—Translating Findings From Humans to Animal Models and Back

Cortisol and Major Depressive Disorder—Translating Findings From Humans to Animal Models and Back

Protective effects of VMY-2-95 on corticosterone-induced injuries in mice and cellular models

Short-term elevations in glucocorticoids do not alter telomere lengths: A systematic review and meta-analysis of non-primate vertebrate studies

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