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Cells
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Chronic Stress Models for Mood Disorders 2020
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Chronic Stress Models for Mood Disorders 2020

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (10 April 2022) | Viewed by 15564

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 significant 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 this 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 fewer 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 behavioral 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 behavioral, cellular, molecular, imaging, 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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26 pages, 10018 KiB  
Article
Experimental Arthritis Inhibits Adult Hippocampal Neurogenesis in Mice
by Kitti Rusznák, Ádám István Horváth, Kinga Pohli-Tóth, Anett Futácsi, Ágnes Kemény, Gabriella Kiss, Zsuzsanna Helyes and Boldizsár Czéh
Cells 2022, 11(5), 791; https://doi.org/10.3390/cells11050791 - 24 Feb 2022
Cited by 6 | Viewed by 3088
Abstract
Background: Adult-born neurons of the hippocampal dentate gyrus play a role in specific forms of learning, and disturbed neurogenesis seems to contribute to the development of neuropsychiatric disorders, such as major depression. Neuroinflammation inhibits adult neurogenesis, but the effect of peripheral inflammation on [...] Read more.
Background: Adult-born neurons of the hippocampal dentate gyrus play a role in specific forms of learning, and disturbed neurogenesis seems to contribute to the development of neuropsychiatric disorders, such as major depression. Neuroinflammation inhibits adult neurogenesis, but the effect of peripheral inflammation on this form of neuroplasticity is ambiguous. Objective: Our aim was to investigate the influence of acute and chronic experimental arthritis on adult hippocampal neurogenesis and to elucidate putative regulatory mechanisms. Methods: Arthritis was triggered by subcutaneous injection of complete Freund’s adjuvant (CFA) into the hind paws of adult male mice. The animals were killed either seven days (acute inflammation) or 21 days (chronic inflammation) after the CFA injection. Behavioral tests were used to demonstrate arthritis-related hypersensitivity to painful stimuli. We used in vivo bioluminescence imaging to verify local inflammation. The systemic inflammatory response was assessed by complete blood cell counts and by measurement of the cytokine/chemokine concentrations of TNF-α, IL-1α, IL-4, IL-6, IL-10, KC and MIP-2 in the inflamed hind limbs, peripheral blood and hippocampus to characterize the inflammatory responses in the periphery and in the brain. In the hippocampal dentate gyrus, the total number of newborn neurons was determined with quantitative immunohistochemistry visualizing BrdU- and doublecortin-positive cells. Microglial activation in the dentate gyrus was determined by quantifying the density of Iba1- and CD68-positive cells. Results: Both acute and chronic arthritis resulted in paw edema, mechanical and thermal hyperalgesia. We found phagocytic infiltration and increased levels of TNF-α, IL-4, IL-6, KC and MIP-2 in the inflamed hind paws. Circulating neutrophil granulocytes and IL-6 levels increased in the blood solely during the acute phase. In the dentate gyrus, chronic arthritis reduced the number of doublecortin-positive cells, and we found increased density of CD68-positive macrophages/microglia in both the acute and chronic phases. Cytokine levels, however, were not altered in the hippocampus. Conclusions: Our data suggest that acute peripheral inflammation initiates a cascade of molecular and cellular changes that eventually leads to reduced adult hippocampal neurogenesis, which was detectable only in the chronic inflammatory phase. Full article
(This article belongs to the Special Issue Chronic Stress Models for Mood Disorders 2020)
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12 pages, 1695 KiB  
Article
Angiotensinergic Neurotransmissions in the Medial Amygdala Nucleus Modulate Behavioral Changes in the Forced Swimming Test Evoked by Acute Restraint Stress in Rats
by Camila Marchi-Coelho, Willian Costa-Ferreira, Lilian L. Reis-Silva and Carlos C. Crestani
Cells 2021, 10(5), 1217; https://doi.org/10.3390/cells10051217 - 17 May 2021
Cited by 3 | Viewed by 2476
Abstract
We investigated the role of angiotensin II type 1 (AT1 receptor) and type 2 (AT2 receptor) and MAS receptors present in the medial amygdaloid nucleus (MeA) in behavioral changes in the forced swimming test (FST) evoked by acute restraint stress in [...] Read more.
We investigated the role of angiotensin II type 1 (AT1 receptor) and type 2 (AT2 receptor) and MAS receptors present in the medial amygdaloid nucleus (MeA) in behavioral changes in the forced swimming test (FST) evoked by acute restraint stress in male rats. For this, rats received bilateral microinjection of either the selective AT1 receptor antagonist losartan, the selective AT2 receptor antagonist PD123319, the selective MAS receptor antagonist A-779, or vehicle 10 min before a 60 min restraint session. Then, behavior in the FST was evaluated immediately after the restraint (15 min session) and 24 h later (5 min session). The behavior in the FST of a non-stressed group was also evaluated. We observed that acute restraint stress decreased immobility during both sessions of the FST in animals treated with vehicle in the MeA. The decreased immobility during the first session was inhibited by intra-MeA administration of PD123319, whereas the effect during the second session was not identified in animals treated with A-779 into the MeA. Microinjection of PD123319 into the MeA also affected the pattern of active behaviors (i.e., swimming and climbing) during the second session of the FST. Taken together, these results indicate an involvement of angiotensinergic neurotransmissions within the MeA in behavioral changes in the FST evoked by stress. Full article
(This article belongs to the Special Issue Chronic Stress Models for Mood Disorders 2020)
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18 pages, 3268 KiB  
Article
Increasing Adult Hippocampal Neurogenesis Promotes Resilience in a Mouse Model of Depression
by Barbara Planchez, Natalia Lagunas, Anne-Marie Le Guisquet, Marc Legrand, Alexandre Surget, René Hen and Catherine Belzung
Cells 2021, 10(5), 972; https://doi.org/10.3390/cells10050972 - 21 Apr 2021
Cited by 20 | Viewed by 4582
Abstract
Many studies evaluated the functional role of adult hippocampal neurogenesis (AHN) and its key role in cognitive functions and mood regulation. The effects of promoting AHN on the recovery of stress-induced symptoms have been well studied, but its involvement in stress resilience remains [...] Read more.
Many studies evaluated the functional role of adult hippocampal neurogenesis (AHN) and its key role in cognitive functions and mood regulation. The effects of promoting AHN on the recovery of stress-induced symptoms have been well studied, but its involvement in stress resilience remains elusive. We used a mouse model enabling us to foster AHN before the exposure to unpredictable chronic mild stress (UCMS) to evaluate the potential protective effects of AHN on stress, assessing the depressive-like phenotype and executive functions. For this purpose, an inducible transgenic mouse model was used to delete the pro-apoptotic gene Bax from neural progenitors four weeks before UCMS, whereby increasing the survival of adult-generated neurons. Our results showed that UCMS elicited a depressive-like phenotype, highlighted by a deteriorated coat state, a higher immobility duration in the tail suspension test (TST), and a delayed reversal learning in a water maze procedure. Promoting AHN before UCMS was sufficient to prevent the development of stressed-induced behavioral changes in the TST and the water maze, reflecting an effect of AHN on stress resilience. Taken together, our data suggest that increasing AHN promotes stress resilience on some depressive-like symptoms but also in cognitive symptoms, which are often observed in MD. Full article
(This article belongs to the Special Issue Chronic Stress Models for Mood Disorders 2020)
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14 pages, 3219 KiB  
Article
Ablation of NPFFR2 in Mice Reduces Response to Single Prolonged Stress Model
by Ya-Tin Lin, Yi-Ling Huang, Sze-Chi Tsai and Jin-Chung Chen
Cells 2020, 9(11), 2479; https://doi.org/10.3390/cells9112479 - 14 Nov 2020
Cited by 10 | Viewed by 2542
Abstract
Mental stress is highly related to many clinical symptoms and disorders, as it activates the hypothalamic-pituitary-adrenocortical (HPA) axis to affect a wide variety of physiological functions. Furthermore, stress leads to the aberrations in HPA axis activity and disruptions of body homeostasis. It was [...] Read more.
Mental stress is highly related to many clinical symptoms and disorders, as it activates the hypothalamic-pituitary-adrenocortical (HPA) axis to affect a wide variety of physiological functions. Furthermore, stress leads to the aberrations in HPA axis activity and disruptions of body homeostasis. It was previously shown that neuropeptide FF (NPFF) regulates the HPA axis through the activation of hypothalamus paraventricular nucleus (PVN), and genetic overexpression or pharmacological stimulation of NPFF receptor 2 (NPFFR2) triggers hyperactivity of HPA axis and suppresses behavioral correlates of emotion in mice. In this study, we further examined the role of NPFFR2 in stress response in mice by utilizing a single prolonged stress (SPS). SPS is considered a model of post-traumatic stress disorder (PTSD), and mice undergo physical restraint, forced swimming, and ether anesthesia within a day followed by social isolation for one week. NPFFR2 knockout B6 mice were generated by CRISPR/Cas9 technology and exposed to SPS. The NPFFR2 knockouts showed resistance to stress exposure-induced anxiety-like behaviors and HPA axis hyperactivity. Additionally, the hippocampal mRNA levels of glucocorticoid receptor and mineralocorticoid receptor were reduced in wild-type (WT) mice but not in NPFFR2 knockouts after stress exposure. Our data also suggested that NPFFR2 knockout mice have stronger negative feedback on the HPA axis after exposure to SPS. Mice with intra-PVN Npffr2 shRNA injection displayed trends toward resistance to SPS exposure in both behavioral and molecular assays. Together, our findings suggest that NPFFR2 may be a potential therapeutic target for disorders relating to stress/anxiety and HPA dysregulation. Full article
(This article belongs to the Special Issue Chronic Stress Models for Mood Disorders 2020)
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Review

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15 pages, 759 KiB  
Review
MAOA uVNTR Genetic Variant and Major Depressive Disorder: A Systematic Review
by Ana Beatriz Castro Gonçalves, Caroline Ferreira Fratelli, Jhon Willatan Saraiva Siqueira, Ligia Canongia de Abreu Cardoso Duarte, Aline Ribeiro Barros, Isabella Possatti, Maurício Lima dos Santos, Calliandra Maria de Souza Silva and Izabel Cristina Rodrigues da Silva
Cells 2022, 11(20), 3267; https://doi.org/10.3390/cells11203267 - 17 Oct 2022
Cited by 4 | Viewed by 1931
Abstract
Major Depressive Disorder (MDD) is a highly prevalent multifactorial psychopathology affected by neurotransmitter levels. Monoamine Oxidase A (MAOA) influences several neural pathways by modulating these levels. This systematic review (per PRISMA protocol and PECOS strategy) endeavors to understand the MAOA uVNTR polymorphism influence [...] Read more.
Major Depressive Disorder (MDD) is a highly prevalent multifactorial psychopathology affected by neurotransmitter levels. Monoamine Oxidase A (MAOA) influences several neural pathways by modulating these levels. This systematic review (per PRISMA protocol and PECOS strategy) endeavors to understand the MAOA uVNTR polymorphism influence on MDD and evaluate its 3R/3R and 3R* genotypic frequencies fluctuation in MDD patients from different populations. We searched the Web of Science, PubMed, Virtual Health Library, and EMBASE databases for eligible original articles that brought data on genotypic frequencies related to the MAOA uVNTR variant in patients with MDD. We excluded studies with incomplete data (including statistical data), reviews, meta-analyses, and abstracts. Initially, we found 43 articles. After removing duplicates and applying the inclusion/exclusion criteria, seven articles remained. The population samples studied were predominantly Asians, with high 3R and 4R allele frequencies. Notably, we observed higher 3R/3R (female) and 3R* (male) genotype frequencies in the healthy control groups and higher 4R/4R (female) and 4R* (male) genotype frequencies in the MDD groups in the majority of different populations. Despite some similarities in the articles analyzed, there is still no consensus on the MAOA uVNTR variant’s role in MDD pathogenesis. Full article
(This article belongs to the Special Issue Chronic Stress Models for Mood Disorders 2020)
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