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Cells
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Chronic Stress Models for Mood Disorders
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Chronic Stress Models for Mood Disorders

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (15 July 2020) | Viewed by 24884

Special Issue Editor

Prof. Boldizsár Czéh

E-Mail Website
Guest Editor
Neurobiology of Stress Research Group, Szentágothai János Research Centre, University of Pécs, Pécs, Hungary
Interests: stress; animal model; depressive disorder; hippocampus; prefrontal cortex; adult neurogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Major depressive disorder is a major public health concern, as it is a common and often recurring condition associated with considerable functional impairments, diminished quality of life, increased medical morbidity, and mortality. Currently, the WHO predicts that by 2030, major depressive disorder will be the largest contributor to the global disease burden. Despite extensive research efforts, the exact pathophysiology of the disorder is still unknown. Effective antidepressants are available, but many of them act too slowly, and patient compliance is hindered by the numerous side effects. Animal models for depression may help us to understand the underlying pathophysiology and to develop novel, faster acting drugs with less side effects. As stress is a major contributor to the development of depressive disorders, animal models based on chronic stress exposure are the most widely used models in research to mimic the depressed behavioural phenotype.
This Special Issue will provide an open-access opportunity for publishing research studies or review articles related to animal models based on chronic stress to mirror depressive disorders. All kinds of studies, including behavioural, cellular, molecular, electrophysiological, or pharmacological studies, are welcome from researchers who work on these topics.

Prof. Boldizsár Czéh
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • animal model
  • chronic mild stress
  • depression
  • learned helplessness
  • mood disorder

Related Special Issue

Published Papers (5 papers)

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Research

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17 pages, 2390 KiB  
Article
Depression-Associated Gene Negr1-Fgfr2 Pathway Is Altered by Antidepressant Treatment
by Lucia Carboni, Francesca Pischedda, Giovanni Piccoli, Mario Lauria, Laura Musazzi, Maurizio Popoli, Aleksander A. Mathé and Enrico Domenici
Cells 2020, 9(8), 1818; https://doi.org/10.3390/cells9081818 - 31 Jul 2020
Cited by 13 | Viewed by 3860
Abstract
The Negr1 gene has been significantly associated with major depression in genetic studies. Negr1 encodes for a cell adhesion molecule cleaved by the protease Adam10, thus activating Fgfr2 and promoting neuronal spine plasticity. We investigated whether antidepressants modulate the expression of genes belonging [...] Read more.
The Negr1 gene has been significantly associated with major depression in genetic studies. Negr1 encodes for a cell adhesion molecule cleaved by the protease Adam10, thus activating Fgfr2 and promoting neuronal spine plasticity. We investigated whether antidepressants modulate the expression of genes belonging to Negr1-Fgfr2 pathway in Flinders sensitive line (FSL) rats, in a corticosterone-treated mouse model of depression, and in mouse primary neurons. Negr1 and Adam10 were the genes mostly affected by antidepressant treatment, and in opposite directions. Negr1 was down-regulated by escitalopram in the hypothalamus of FSL rats, by fluoxetine in the hippocampal dentate gyrus of corticosterone-treated mice, and by nortriptyline in hippocampal primary neurons. Adam10 mRNA was increased by nortriptyline administration in the hypothalamus, by escitalopram in the hippocampus of FSL rats, and by fluoxetine in mouse dorsal dentate gyrus. Similarly, nortriptyline increased Adam10 expression in hippocampal cultures. Fgfr2 expression was increased by nortriptyline in the hypothalamus of FSL rats and in hippocampal neurons. Lsamp, another IgLON family protein, increased in mouse dentate gyrus after fluoxetine treatment. These findings suggest that Negr1-Fgfr2 pathway plays a role in the modulation of synaptic plasticity induced by antidepressant treatment to promote therapeutic efficacy by rearranging connectivity in corticolimbic circuits impaired in depression. Full article
(This article belongs to the Special Issue Chronic Stress Models for Mood Disorders)
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17 pages, 2363 KiB  
Article
Serum Level of miR-1 and miR-155 as Potential Biomarkers of Stress-Resilience of NET-KO and SWR/J Mice
by Joanna Solich, Maciej Kuśmider, Agata Faron-Górecka, Paulina Pabian, Magdalena Kolasa, Beata Zemła and Marta Dziedzicka-Wasylewska
Cells 2020, 9(4), 917; https://doi.org/10.3390/cells9040917 - 9 Apr 2020
Cited by 11 | Viewed by 2827
Abstract
In the present study, we used three strains of mice with various susceptibility to stress: mice with knock-out of the gene encoding norepinephrine transporter (NET-KO), which are well characterized as displaying a stress-resistant phenotype, as well as two strains of mice displaying two [...] Read more.
In the present study, we used three strains of mice with various susceptibility to stress: mice with knock-out of the gene encoding norepinephrine transporter (NET-KO), which are well characterized as displaying a stress-resistant phenotype, as well as two strains of mice displaying two different stress-coping strategies, i.e., C57BL/6J (WT in the present study) and SWR/J. The procedure of restraint stress (RS, 4 h) was applied, and the following behavioral experiments (the forced swim test and sucrose preference test) indicated that NET-KO and SWR/J mice were less sensitive to RS than WT mice. Then, we aimed to find the miRNAs which changed in similar ways in the serum of NET-KO and SWR/J mice subjected to RS, being at the same time different from the miRNAs found in the serum of WT mice. Using Custom TaqMan Array MicroRNA Cards, with primers for majority of miRNAs expressed in the serum (based on a preliminary experiment using the TaqMan Array Rodent MicroRNA A + B Cards Set v3.0, Thermo Fisher Scientific, Waltham, MA, USA) allowed the identification of 21 such miRNAs. Our further analysis focused on miR-1 and miR-155 and their targets—these two miRNAs are involved in the regulation of BDNF expression and can be regarded as biomarkers of stress-resilience. Full article
(This article belongs to the Special Issue Chronic Stress Models for Mood Disorders)
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17 pages, 2357 KiB  
Article
Deficiency in Androgen Receptor Aggravates the Depressive-Like Behaviors in Chronic Mild Stress Model of Depression
by Yi-Yung Hung, Ya-Ling Huang, Chawnshang Chang and Hong-Yo Kang
Cells 2019, 8(9), 1021; https://doi.org/10.3390/cells8091021 - 2 Sep 2019
Cited by 29 | Viewed by 4381
Abstract
While androgen receptor (AR) and stress may influence the development of the major depressive disorder (MDD), the detailed relationship, however, remains unclear. Here we found loss of AR accelerated development of depressive-like behaviors in mice under chronic mild stress (CMS). Mechanism dissection indicated [...] Read more.
While androgen receptor (AR) and stress may influence the development of the major depressive disorder (MDD), the detailed relationship, however, remains unclear. Here we found loss of AR accelerated development of depressive-like behaviors in mice under chronic mild stress (CMS). Mechanism dissection indicated that AR might function via altering the expression of miR-204-5p to modulate the brain-derived neurotrophic factor (BDNF) expression to influence the depressive-like behaviors in the mice under the CMS. Adding the antiandrogen flutamide with the stress hormone corticosterone can additively decrease BDNF mRNA in mouse hippocampus mHippoE-14 cells, which can then be reversed via down-regulating the miR-204-5p expression. Importantly, targeting this newly identified AR-mediated miR-204-5p/BDNF/AKT/MAPK signaling with small molecules including 7,8-DHF and fluoxetine, all led to alter the depressive-like behavior in AR knockout mice under CMS exposure. Together, results from these preclinical studies conclude that decreased AR may accelerate the stress-induced MDD via altering miR-204-5p/BDNF/AKT/MAPK signaling, and targeting this newly identified signaling may help in the development of better therapeutic approaches to reduce the development of MDD. Full article
(This article belongs to the Special Issue Chronic Stress Models for Mood Disorders)
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14 pages, 3907 KiB  
Article
Effect of Chronic Corticosterone Treatment on Depression-Like Behavior and Sociability in Female and Male C57BL/6N Mice
by Stefanie Berger, Sarah Gureczny, Sonali N. Reisinger, Orsolya Horvath and Daniela D. Pollak
Cells 2019, 8(9), 1018; https://doi.org/10.3390/cells8091018 - 1 Sep 2019
Cited by 32 | Viewed by 6010
Abstract
Depression is a very common psychiatric disorder affecting approximately 300 million people worldwide with the prevalence being twice as high in women as in men. Despite intense research efforts in recent decades, the neurobiological basis underlying depression remains incompletely understood. However, the exposure [...] Read more.
Depression is a very common psychiatric disorder affecting approximately 300 million people worldwide with the prevalence being twice as high in women as in men. Despite intense research efforts in recent decades, the neurobiological basis underlying depression remains incompletely understood. However, the exposure to chronic stress is widely accepted to constitute a precipitating factor for the development of this mental disorder. Several animal models for the investigation of the pathogenetic link between chronic stress and depression exist and have yielded important insights. The present study aimed at comparing two published protocols for the induction of depression-like behavior in mice based on chronic oral glucocorticoid application. Given the gender distribution in the prevalence of depression, the second goal of this study was to reveal possible differences in the behavioral responses of female and male mice to corticosterone (CORT) treatment. CORT treatment was found to modulate depression-like behavior in selected behavioral paradigms in a sex- and protocol-specific manner. These data are of relevance for the experimental design and interpretation of future studies in the field and further highlight the relevance of “sex as biological variable” to be considered an important parameter for experimental planning and interpretation of results. Full article
(This article belongs to the Special Issue Chronic Stress Models for Mood Disorders)
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Review

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26 pages, 2217 KiB  
Review
Stress-Induced Morphological, Cellular and Molecular Changes in the Brain—Lessons Learned from the Chronic Mild Stress Model of Depression
by Ahmad Raza Khan, Lili Geiger, Ove Wiborg and Boldizsár Czéh
Cells 2020, 9(4), 1026; https://doi.org/10.3390/cells9041026 - 21 Apr 2020
Cited by 37 | Viewed by 7312
Abstract
Major depressive disorder (MDD) is a severe illness imposing an increasing social and economic burden worldwide. Numerous rodent models have been developed to investigate the pathophysiology of MDD. One of the best characterized and most widely used models is the chronic mild stress [...] Read more.
Major depressive disorder (MDD) is a severe illness imposing an increasing social and economic burden worldwide. Numerous rodent models have been developed to investigate the pathophysiology of MDD. One of the best characterized and most widely used models is the chronic mild stress (CMS) model which was developed more than 30 years ago by Paul Willner. More than 2000 published studies used this model, mainly to assess novel compounds with potential antidepressant efficacy. Most of these studies examined the behavioral consequences of stress and concomitant drug intervention. Much fewer studies focused on the CMS-induced neurobiological changes. However, the stress-induced cellular and molecular changes are important as they may serve as potential translational biomarkers and increase our understanding of the pathophysiology of MDD. Here, we summarize current knowledge on the structural and molecular alterations in the brain that have been described using the CMS model. We discuss the latest neuroimaging and postmortem histopathological data as well as molecular changes including recent findings on microRNA levels. Different chronic stress paradigms occasionally deliver dissimilar findings, but the available experimental data provide convincing evidence that the CMS model has a high translational value. Future studies examining the neurobiological changes in the CMS model in combination with clinically effective antidepressant drug intervention will likely deliver further valuable information on the pathophysiology of MDD. Full article
(This article belongs to the Special Issue Chronic Stress Models for Mood Disorders)
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