Repeated exposure to corticosterone increases depression-like behavior in two different versions of the forced swim test without altering nonspecific locomotor activity or muscle strength

Marks, Wendie N.; Fournier, Neil M.; Kalynchuk, Lisa E.

doi:10.1016/j.physbeh.2009.04.014

Cited by 102 publications

(87 citation statements)

References 34 publications

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“…The problem of identifying the most depression-vulnerable insomnia subtypes Core symptoms of major depression include anhedonia, despair, insomnia and cognitive impairment, along with frequent anxiety and comorbid diseases [29,30] . In an animal model, the increased immobility behavior in the FST is considered to be an indicator of despair and sucrose preference is considered to be an index of anhedonia [16,17,20] . In this study, we used a repetitive CORT treatment paradigm to mimic stress-induced sleep disorders.…”

Section: Discussionmentioning

confidence: 99%

“…In this experiment, FST was performed according to a modified version of the paradigm [16,17] . After sleep recording, each rat was placed individually, for 5 min, into a 25 cm diameter×60 cm height Plexiglas cylinder filled with 23-25 °C water to a depth of 40 cm.…”

Section: Forced Swim Testmentioning

confidence: 99%

“…Repeated administration of corticosterone (CORT) can mimic the stress response and avoid the individual differences that can occur when an animal is exposed to stressors [15] . Many studies have adopted this paradigm for inducing depressive behaviors in animal models [16,17] .…”

Section: Introductionmentioning

confidence: 99%

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Correlations between depression behaviors and sleep parameters after repeated corticosterone injections in rats

Wang

Zhang

et al. 2014

Acta Pharmacol Sin

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Aim: Disrupted sleep may be a prodromal symptom or a predictor of depressive disorders. In this study we investigated the relationship between depression symptoms and disrupted sleep using a novel model of stress-mimicked sleep disorders in rats. Methods: SD rats were injected with corticosterone (10, 20 or 40 mg/kg, sc) or vehicle for 7 d. Their sleep-wake behavior was monitored through implanted EEG and EMG electrodes. Their depressive behaviors were assessed using forced swim test, open field test and sucrose preference test. Results: The corticosterone-treated rats showed significantly reduced sleep time, disinhibition of rapid-eye-movement (REM) sleep and altered power spectra during non-REM sleep. All depressive behavioral tests did not show significant difference across the groups. However, individual correlation analysis revealed statistically significance: the immobility time (despair) was negatively correlated with REM sleep latency, slow wave sleep (SWS) time ratio, SWS bouts and delta power density, and it was positively correlated with REM sleep bouts and beta power density. Meanwhile, sucrose preference (anhedonia) was positively correlated with total sleep time and light sleep bouts, and it was negatively correlated with the REM sleep time ratio. Conclusion: In stress-mimicked rats, sleep disturbances are a predictor of depressive disorders, and certain symptoms of depression may be related to the disruption of several specific sleep parameters.

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Section: Discussionmentioning

confidence: 99%

Section: Forced Swim Testmentioning

confidence: 99%

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Correlations between depression behaviors and sleep parameters after repeated corticosterone injections in rats

Wang

Zhang

et al. 2014

Acta Pharmacol Sin

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“…Studies have shown that most symptoms of chronic unpredictable stress-induced depression occur due to the impairment of neuroendocrine, anti-oxidant defense, and inflammatory systems (Eren et al, 2007;Mao et al, 200;Marks et al, 2009;You et al, 2011). A study by Schaalan et al (2011), reported neuroendocrine impairment and significant increase in serum adrenocorticotropin and corticosterone levels in mice exposed to chronic unpredictable stress (Schaalan and Nassar, 2011).…”

Section: Discussionmentioning

confidence: 99%

Study of antidepressant effects of grape seed oil in male mice using tail suspension and forced swim tests

Rabiei

Naderi

Rafieian-Kopaei

2017

Bangladesh J Pharmacol

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The aim of this study was to investigate the antidepressant effects of grape seed oil in male mice (n=60) using tail suspension and forced swim tests. Mice were divided to six groups of 10 in each group. Group I: Intraperitoneally receiving normal saline; Group II: Received normal saline & stress; Group III-V: Injected (i.p.) with different (60, 120, and 240 mg/kg) doses of grape seed oil; and Group VI: Received fluoxetine (10 mg/kg). Grape seed oil in 60 mg/kg significantly decreased immobility time in tail suspension and forced swim tests under chronic unpredictable stress compared to groups under chronic stress receiving normal saline and grape seed oil (120 and 240 mg/kg). Grape seed oil (60 mg/kg) significantly improved the motor balance in mice under chronic stress. It had no significant effect on serum corticosterone level. Grape seed oil can improve depression symptoms in mice.Video Clip of Methodology:0 min 14 sec <a href="https://youtube.com/v/7JgyR4mTUOw">Full Screen</a> <a href="https://youtube.com/watch?v=7JgyR4mTUOw">Alternate</a>

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“…Long-term exposure of corticosteroids is associated with a range of actions leading to depressive behaviour [47,48]. Changes in the hippocampus of the brain caused by the extended use of corticosteroids [49][50][51] could be attributed to depressive behaviour. The decrease in sucrose preference can be a manifestation of behavioural changes like anhedonia, seen with chronic use of corticosteroids as documented in previous research [52].…”

Section: Discussionmentioning

confidence: 99%

Role of Aspirin and Dexamethasone against Experimentally Induced Depression in Rats

Bhatt

Shukla

Raval

et al. 2016

Basic Clin Pharma Tox

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A large number of current studies indicate that inflammatory mediators may contribute to depression in experimental models as well as in human beings. Nevertheless, the subject, whether anti-inflammatory treatments can prevent depression still remains controversial. In the present study, a chronic mild stress (CMS) model of male Sprague Dawley rats was used to investigate the role of anti-inflammatory drugs in the treatment of depression. All the animals in different groups, except the normal control group, were exposed to CMS procedure for 28 days and concurrently treated with aspirin (10 mg/kg, p.o.), dexamethasone (1 mg/kg p.o.) and amitriptyline (10 mg/kg p.o., reference standard), respectively. Amitriptyline was also used in combination with aspirin and dexamethasone to inspect any synergistic effects. Tests performed towards the end of the study included sucrose preference test, behavioural tests like forced swim test, elevated plus-maze, light/dark box, locomotor activity and biochemical estimations like serum cortisol and brain neurotransmitters. Disease control group (CMS-treated) produced significant depressive behaviour in rats. The animals treated with aspirin showed increased sucrose preference, decreased immobility time in forced swim test, decreased serum cortisol and increased brain serotonin levels signifying antidepressant action. In contrast, there was aggravation of depressive behaviour in rats treated with dexamethasone. Together, these findings suggest that aspirin can serve as a potential antidepressant both individually and as adjunctive agent in the treatment of depression. Inhibition of the inflammatory mediators during stress procedures or any other potential physiological and biochemical mechanisms may be involved in its antidepressant effect.Major depression is one of the most commonly diagnosed neuropsychiatric disorders, with a worldwide life-time prevalence of 17%. It is estimated that by 2020, major depression will be the second most disabling condition in the world. Despite considerable strides have been made over the years, treatment-resistant depression (TRD) remains a common condition which accounts for approximately 30% of the depressed population [1,2]. Historically, treatment options for depression and associated disorders have focused on the medications that modify the activity of monoamine neurotransmitter systems [3].Several studies support the role of inflammation and immune system deregulation in pathophysiology of depression [4,5]. Patients with major depression have been found to exhibit all of the vital features of inflammation, including elevation of inflammatory cytokines, acute phase proteins, chemokines, adhesion molecules and inflammatory mediators such as prostaglandins. Repeated administration of IL-1, TNF-a and IL-6 elicits depressive-like behaviour in animals [6][7][8]. The mechanisms contributing to pathogenesis of depression incorporate abnormal neurotransmitter metabolism, altered neuro-endocrine functions and distorted neural plasticity [9,10...

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Repeated exposure to corticosterone increases depression-like behavior in two different versions of the forced swim test without altering nonspecific locomotor activity or muscle strength

Cited by 102 publications

References 34 publications

Correlations between depression behaviors and sleep parameters after repeated corticosterone injections in rats

Correlations between depression behaviors and sleep parameters after repeated corticosterone injections in rats

Study of antidepressant effects of grape seed oil in male mice using tail suspension and forced swim tests

Role of Aspirin and Dexamethasone against Experimentally Induced Depression in Rats

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