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A Chronic Immobilization Stress Protocol for Inducing Depression-Like Behavior in Mice
Published on: May 15, 2019
Major depressive disorder mediates accelerated aging in rats subjected to chronic mild stress
Xiaoxian Xie1, Yangyang Chen1, Lingyan Ma1
1College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310032, China.
Abstract:
Major depressive disorder (MDD) has a complex etiology and is characterized by a change in mood and psychophysiological state. MDD has been shown to mediate accelerated biological aging in patients, although the underlying mechanism is not well understood. In the present study, we used a chronic mild stress (CMS) paradigm to induce anhedonia, one of the main symptoms of MDD. CMS induced depression-like symptoms in rats, including reduced sucrose preference and increased immobility time in the forced swim test. Moreover, stressed rats travelled a shorter total distance, had fewer grid line crossings, and spent less time in the outer zone in the open field test than controls. CMS altered the levels of 5-hydroxytryptophan, dopamine, and corticosterone in the serum and hippocampus (P<0.05); these rats also exhibited impaired liver function, decreased telomerase activity, and telomere shortening, which was associated with increased oxidative damage along with decreased superoxide dismutase and glutathione reductase activities. Mitochondria in CMS-treated rats showed ultrastructural damage as well as reduced DNA content and integrity. These findings provide physiological and cellular evidence that the MDD can mediate accelerated aging in rats.
Insights
Major depressive disorder (MDD) accelerates biological aging. Chronic mild stress in rats induced depression-like symptoms, leading to cellular damage and shortened telomeres, supporting MDD
Area of Science:
- Neuroscience
- Gerontology
- Biochemistry
Background:
- Major depressive disorder (MDD) is linked to accelerated biological aging, but mechanisms remain unclear.
- Anhedonia, a key MDD symptom, is often studied using chronic mild stress (CMS) models.
- Understanding MDD's impact on aging is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the physiological and cellular mechanisms by which MDD, induced by CMS, accelerates aging in rats.
- To examine the effects of CMS on depression-like behaviors, neurochemical levels, organ function, and cellular aging markers.
Main Methods:
- Induction of depression-like symptoms in rats using a chronic mild stress (CMS) paradigm.
- Behavioral assessments including sucrose preference, forced swim test, and open field test.
- Biochemical analysis of serum and hippocampal neurotransmitters (e.g., 5-hydroxytryptophan, dopamine) and corticosterone.
- Evaluation of liver function, telomerase activity, telomere length, oxidative stress markers (superoxide dismutase, glutathione reductase), and mitochondrial integrity.
Main Results:
- CMS successfully induced depression-like behaviors in rats.
- Stressed rats showed altered neurotransmitter and corticosterone levels, impaired liver function, and decreased telomerase activity.
- Telomere shortening, increased oxidative damage, and mitochondrial ultrastructural damage were observed in CMS-treated rats.
- These cellular changes correlated with accelerated aging markers.
Conclusions:
- Chronic mild stress in rats leads to physiological and cellular changes indicative of accelerated aging.
- MDD pathogenesis involves mechanisms that contribute to biological aging, including oxidative stress and telomere attrition.
- This study provides evidence linking depression to accelerated aging at both systemic and cellular levels.
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