Effect of a novel 5-HT3 receptor antagonist 4i, in corticosterone-induced depression-like behavior and oxidative stress in mice

Gupta, Deepali; Mahesh, Radhakrishnan; Kurhe, Yeshwant

doi:10.1016/j.steroids.2015.01.021

Cited by 50 publications

(23 citation statements)

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“…Numerous findings have demonstrated that corticosterone causes neurotoxicity, apoptosis [13,42,53], and oxidative stress [54,55]. Based on these findings, our present study was designed to detect the toxicity of corticosterone to PC12 cells.…”

Section: Discussionmentioning

confidence: 98%

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Gao

Zou

et al. 2015

ABBS

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Corticosterone, one of the glucocorticoids, is toxic to neurons and plays an important role in depressive-like behavior and depression. We previously showed that hydrogen sulfide (H 2 S), a novel physiological mediator, plays an inhibitory role in depression. However, the mechanism underlying H 2 S-triggered antidepressant-like role is not clearly known. Brain-derived neurotrophic factor (BDNF), a neurotrophic factor, plays a neuroprotective role that is mediated by its high-affinity tropomysin-related kinase B (TrkB) receptor. In this study, to investigate the underlying mechanism of H 2 S-induced antidepressant-like role, we explored whether H 2 S could protect neurons against corticosterone-mediated cyctotoxicity and whether this protective role of H 2 S was involved in the regulation of BDNF-TrkB pathway. Our data demonstrated that sodium hydrosulfide (NaHS), the donor of H 2 S, could prevent corticosterone-induced cytotoxicity, apoptosis, accumulation of intracellular reactive oxygen species (ROS) and loss of mitochondrial membrane potential (MMP) in PC12 cells. NaHS not only induced the up-regulation of BDNF but also prevented the down-regulation of BDNF by corticosterone. It was also found that blocking BDNF-TrkB pathway by K252a, an inhibitor of TrkB, abolished the protection of H 2 S against corticosterone-induced cytotoxicity, apoptosis, accumulation of ROS, and loss of MMP. These results suggest that H 2 S protects against the neurotoxicity of corticosterone by modulation of the BDNF-TrkB pathway.

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Section: Discussionmentioning

confidence: 98%

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Gao

Zou

et al. 2015

ABBS

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“…Dysregulation of hypothalamic-pituitaryadrenal (HPA) axis has been implicated in the development of depression-like behavior, which remains under diagnosed and poorly treated [8]. Exogenous corticosterone (CORT) administration has been demonstrated to develop a depression model, which has shown to mimic HPA-axis induced depression-like state in rodents [29,18,30].…”

Section: Discussionmentioning

confidence: 99%

“…Stressful life events have demonstrated a substantial causal association with depression and stress paradigms have long been used to model the disease [6][7][8]. Several findings have shown hypothalamic-pituitary-adrenal (HPA) axis dysfunction in stressrelated illnesses, including depression [9,10].…”

Section: Introductionmentioning

confidence: 99%

Resveratrol ameliorates depressive-like behavior in repeated corticosterone-induced depression in mice

et al. 2015

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“…High levels of serum cortisol, related to elevated hypothalamo‐pituitary‐adrenal (HPA) axis activity, can be associated with depression. The CORT model tests the pharmacologically evoked anxio‐depressive state in animals by application of corticosterone, the rodent functional analogue of cortisol (Krugers, Lucassen, Karst, & Joels, ; Rosa et al, ) where corticosterone are subcutaneously applied on daily basis for two, three, five, or eight weeks (Gupta, Radhakrishnan, & Kurhe, ; Kv et al, ; Schloesser et al, ; Zhang et al, ). The OB models chronic agitated hypo‐serotonergic depression in mice (Lumia, Teicher, Salchli, Ayers, & Possidente, ).…”

Section: Introductionmentioning

confidence: 99%

Long‐term stability and characteristics of behavioral, biochemical, and molecular markers of three different rodent models for depression

et al. 2019

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Objective:The present study was designed to explore the long-term differences between three mouse models for depression. Method:In the present study, the unpredictable chronic mild stress (UCMS) model, the glucocorticoid/corticosterone model, and the olfactory bulbectomy model were compared at two, three, and five weeks after model induction. Behavioral testing performed included forced-swimming, tail suspension, open-field and elevated plusmaze tests. In addition, 5-hydroxytryptamine (5-HT) and dopamine levels, and mRNA and protein expressions related to 5-HT synthesis, transport, and signaling were analyzed in the hippocampus of tested animals. Results:Our results revealed that each model demonstrated a specific profile of markers, whereas the stability of them differed over testing time. Conclusions:Each model provided a unique set of advantages that can be considered depending on the context and aims of each study. Among the three models, the UCMS model was mostly stable and appeared to the best model for testing long-term depression-like state. K E Y W O R D S 5-HT, corticosterone, depression model, glucocorticoid, olfactory bulbectomy, UCMS How to cite this article: Zhu H, Tao Y, Wang T, et al. Long-term stability and characteristics of behavioral, biochemical, and molecular markers of three different rodent models for depression. Brain Behav. 2020;10:e01508. https ://doi.

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Effect of a novel 5-HT3 receptor antagonist 4i, in corticosterone-induced depression-like behavior and oxidative stress in mice

Cited by 50 publications

References 54 publications

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Resveratrol ameliorates depressive-like behavior in repeated corticosterone-induced depression in mice

Long‐term stability and characteristics of behavioral, biochemical, and molecular markers of three different rodent models for depression

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Effect of a novel 5-HT3 receptor antagonist 4i, in corticosterone-induced depression-like behavior and oxidative stress in mice

Cited by 50 publications

References 54 publications

H&lt;sub&gt;2&lt;/sub&gt;S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

H&lt;sub&gt;2&lt;/sub&gt;S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Resveratrol ameliorates depressive-like behavior in repeated corticosterone-induced depression in mice

Long‐term stability and characteristics of behavioral, biochemical, and molecular markers of three different rodent models for depression

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H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway