scholarly journals The Effect of Swimming on Anxiety-Like Behaviors and Corticosterone in Stressed and Unstressed Rats

Author(s):  
Mohammad Amin Safari ◽  
Maryam Koushkie Jahromi ◽  
Rasoul Rezaei ◽  
Hadi Aligholi ◽  
Serge Brand

This study assessed the effect of swimming training on anxiety-like behaviors and corticosterone. Thirty adult male Wistar rats were randomly assigned to five study conditions: swimming training (ST); exposure to chronic mild stress (CS); exposure to chronic mild stress followed by swimming training (CS + ST); exposure to chronic mild stress followed by a recovery period (CS + recovery); control. The exercise training consisted of 60 min of swimming exercise per day, for five days a week, and four consecutive weeks. A chronic mild stress program (CMS) was applied for a period of four weeks. Anxiety-like behaviors were measured by open field test (OFT). The number of excrements and blood corticosterone were used as physiological parameters of anxiety. To assess corticosterone, blood samples were taken 48 h after the last session of experiments. Compared to other study conditions, the lowest anxiety-like behaviors and corticosterone concentrations were observed in the ST condition in unstressed rats. In stressed rats, as in the ST + CS group, swimming training probably reduced some anxiety behaviors, but the results showed increased corticosterone compared to control and CS + Recovery. Anxiety parameters and corticosterone concentrations were greatest in the CS condition. In the ST group, anxiety parameters were less than for the ST + CS group. In the CS + Recovery group, anxiety parameters were less than for the CS group. In summary, self-paced swimming training could attenuate some anxiety parameters in both stressed and non-stressed rats. The effect of swimming training in unstressed rats was more prominent than in stressed rats. In stressed rats, a period of recovery was more effective than swimming training in reducing corticosterone. Mechanisms of anxiety reduction other than cortisol should be investigated in future research.

2016 ◽  
Vol 33 (S1) ◽  
pp. S527-S527
Author(s):  
D. Martín Hernández ◽  
Á.G. Bris ◽  
K.S. MacDowell ◽  
A. Sayd ◽  
D. Azpiazu ◽  
...  

IntroductionPatients with major depression who are otherwise medically healthy have activated inflammatory pathways. It has been described that depression is not only escorted by inflammation but also by induction of multiple oxidative/nitrosative stress pathways. Nevertheless, there are finely regulated mechanisms involved in preserving cells from damage, such as the nuclear factor Nrf2.AimsTo explore in a depression-like model the Nrf2 pathway in the prefrontal cortex (PFC) and the hippocampus of rats and to analyze which classic antidepressants affect the antioxidant activity of the Nrf2 pathway.MethodsMale Wistar rats were exposed to chronic mild stress (CMS) and some of them were treated with desipramine, escitalopram or duloxetine. We studied the expression in the PFC and hippocampus of upstream and downstream elements of the Nrf2 pathway and the oxidative damage induced by the CMS.ResultsAfter exposure to a CMS protocol, in the PFC, there is an inhibition of upstream and downstream elements of the Nrf2 pathway. Moreover, antidepressant treatments, particularly desipramine and duloxetine, are able to recover some of these elements and to reduce the oxidative damage induced by the depression model. In the hippocampus however, Nrf2 pathways are not that affected and antidepressants do not have many actions.ConclusionsNrf2 pathway is differentially regulated by antidepressants in the PFC and hippocampus. The Nrf2 pathway is involved in the oxidative/nitrosative damage detected in the PFC after CMS exposure. However, it seems that Nrf2 is not very involved in the effects caused by the CMS in the hippocampus.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Ru-Peng Liu ◽  
Ji-Liang Fang ◽  
Pei-Jing Rong ◽  
Yufeng Zhao ◽  
Hong Meng ◽  
...  

To explore new noninvasive treatment options for depression, this study investigated the effects of electroacupuncture (EA) at the auricular concha region (ACR) of depression rat models. Depression in rats was induced by unpredictable chronic mild stress (UCMS) combined with isolation for 21 days. Eighty male Wistar rats were randomly assigned into four groups: normal, UCMS alone, UCMS with EA-ACR treatment, and UCMS with EA-ear-tip treatment. Rats under inhaled anesthesia were treated once daily for 14 days. The results showed that blood pressure and heart rate were significantly reduced in the EA-ACR group than in the UCMS alone group or the EA-ear-tip group. The open-field test scores significantly decreased in the UCMS alone and EA-ear-tip groups but not in the EA-ACR group. Both EA treatments downregulated levels of plasma cortisol and ACTH in UCMS rats back to normal levels. The present study suggested that EA-ACR can elicit similar cardioinhibitory effects as vagus nerve stimulation (VNS), and EA-ACR significantly antagonized UCMS-induced depressive status in UCMS rats. The antidepressant effect of EA-ACR is possibly mediated via the normalization of the hypothalamic-pituitary-adrenal (HPA) axis hyperactivity.


2007 ◽  
Vol 87 (1) ◽  
pp. 130-140 ◽  
Author(s):  
Ying Pan ◽  
Ling-Dong Kong ◽  
Yu-Cheng Li ◽  
Xing Xia ◽  
Hsiang-Fu Kung ◽  
...  

2017 ◽  
Vol 321 ◽  
pp. 137-147 ◽  
Author(s):  
J.J. Herrera-Pérez ◽  
L. Martínez-Mota ◽  
G. Jiménez-Rubio ◽  
L. Ortiz-López ◽  
E.A. Cabrera-Muñoz ◽  
...  

2019 ◽  
Vol 33 (6) ◽  
pp. 748-756 ◽  
Author(s):  
Mariusz Papp ◽  
Piotr Gruca ◽  
Magdalena Lason ◽  
Monika Niemczyk ◽  
Paul Willner

Aims: The Wistar-Kyoto rat has been validated as an animal model of treatment-resistant depression. Here we investigated a role of dopamine D2 and D3 receptors in the ventro-medial prefrontal cortex in the mechanism of action of deep brain stimulation in Wistar-Kyoto rats and venlafaxine in Wistar rats. Methods: Wistar or Wistar-Kyoto rats were exposed chronically to chronic mild stress. Wistar rats were treated chronically with venlafaxine (10 mg/kg) beginning after two weeks of chronic mild stress; Wistar-Kyoto rats received two sessions of deep brain stimulation before behavioural tests. L-742,626 (1 µg), a D2 receptor agonist, or 7-OH DPAT (3 µg), a D3 receptor antagonist, were infused into the ventro-medial prefrontal cortex immediately following the exposure trial in the Novel Object Recognition Test, and discrimination between novel and familiar object was tested one hour later. Results: Chronic mild stress decreased sucrose intake and impaired memory consolidation; these effects were reversed by venlafaxine in Wistar rats and deep brain stimulation in Wistar-Kyoto rats. In control animals, L-742,626 and 7-OH DPAT also impaired memory consolidation. In Wistar rats, venlafaxine reversed the effect of L-742,626 in controls, but not in the chronic mild stress group, and venlafaxine did not reverse the effect of 7-OH DPAT in either group. In Wistar-Kyoto rats, deep brain stimulation reversed the effect of both L-742,626 and 7-OH DPAT in both control and chronic mild stress groups. Conclusions: We conclude that the action of venlafaxine to reverse the impairment of memory consolidation caused by chronic mild stress in Wistar rats involves D2 receptors in the ventro-medial prefrontal cortex; but the effect of deep brain stimulation to reverse the same effect in Wistar-Kyoto rats does not.


2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Yu Zhang ◽  
Feng Shao ◽  
Qiong Wang ◽  
Xi Xie ◽  
Weiwen Wang

Using a valid chronic mild stress (CMS) model of depression, we found that adolescent (postnatal days [PND] 28–41) CMS induced transient alterations in anhedonia that did not persist into adulthood after a 3-week recovery period. Previously stressed adult rats exhibited more immobility/despair behaviors in the forced swimming test and a greater number of trials to reach criterion in the set-shifting task, suggesting the impaired ability to cope with stressors and the cognitive flexibility that allows adaptation to dynamic environments during adulthood. In addition, adult rat exposure to adolescent CMS had a relatively inhibited activation in ERK signaling and downstream protein expression of phosphorylated cAMP-response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) in the medial prefrontal cortex. Further correlation analysis demonstrated that immobility and set-shifting performance were positively correlated with the inhibition of ERK signaling. These results indicated adolescent CMS can be used as an effective stressor to model an increased predisposition to adult depression.


Alcohol ◽  
2017 ◽  
Vol 63 ◽  
pp. 43-51 ◽  
Author(s):  
Priscila Vázquez-León ◽  
Lucía Martínez-Mota ◽  
Lucía Quevedo-Corona ◽  
Abraham Miranda-Páez

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