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Stress-Related Disorders and Depression: From Molecular Basis to Therapy (2nd Edition)

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 November 2024 | Viewed by 3850

Special Issue Editors

Prof. Dr. Irena Nalepa

E-Mail Website
Guest Editor
Department of Brain Biochemistry, Maj Institute of Pharmacology of the Polish Academy of Sciences, Smętna 12, 31-343 Krakow, Poland
Interests: neuroscience; neuropharmacology; stress-related disorders; depression; psychotropic drugs; GPCR signaling; noradrenergic system; neuroplasticity, neuroimmune interaction
Special Issues, Collections and Topics in MDPI journals
Dr. Agnieszka Zelek-Molik

E-Mail Website
Guest Editor
Department of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343 Kraków, Poland
Interests: neurobiology; pharmacology; stress; psychiatric disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Stress is defined as a challenge to the homeostasis of an organism by events coming from the environment. Two major systems are essential in the response to stressors: the sympathetic adrenomedullary system and the hypothalamic–pituitary–adrenal axis (HPA). Elevated by stress, noradrenaline and HPA axis-related hormones (including CRH, vasopressin, ACTH, corticosteroids) influence the gene transcription processes and the functioning of neurotransmitter systems. The immune system’s responsiveness is also affected. Via alterations to brain structure, chemistry, and function, chronic stress contributes to depression and various anxiety disorders, including posttraumatic stress disorder (PTSD). There is evidence demonstrating that chronic stress may also contribute to addiction and obesity.

The purpose of this Special Issue is to collect original research articles and review papers that concern the study of how the brain transduces environmental stress exposure into depression and stress-related diseases. We aim to bring together the most recent studies and use different experimental approaches, in vivo or in vitro, for the purpose of addressing:

  1. molecular and cellular responses to stress;
  2. stress-induced changes in the neurochemical cross-talk between signaling systems in the brain;
  3. methods to study the effects of various stressors in psychiatric disease models;
  4. stress vulnerability and resilience;
  5. stress biomarkers;
  6. therapies for stress-related disorders.

Prof. Dr. Irena Nalepa
Dr. Agnieszka Zelek-Molik
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • psychobiology of stress
  • depression
  • posttraumatic stress disorder
  • anxiety disorders
  • animal models
  • biogenic monoamines
  • glucocorticoids
  • inflammation
  • antidepressant and anxiolytic drugs

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Published Papers (3 papers)

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Research

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23 pages, 2417 KiB  
Article
Postpartum Oxytocin Treatment via the Mother Reprograms Long-Term Behavioral Disorders Induced by Early Life Stress on the Plasma and Brain Metabolome in the Rat
by Sara Morley-Fletcher, Alessandra Gaetano, Vance Gao, Eleonora Gatta, Gilles Van Camp, Hammou Bouwalerh, Pierre Thomas, Ferdinando Nicoletti and Stefania Maccari
Int. J. Mol. Sci. 2024, 25(5), 3014; https://doi.org/10.3390/ijms25053014 - 5 Mar 2024
Cited by 1 | Viewed by 1195
Abstract
The rat model of perinatal stress (PRS), in which exposure of pregnant dams to restraint stress reduces maternal behavior, is characterized by a metabolic profile that is reminiscent of the “metabolic syndrome”. We aimed to identify plasma metabolomic signatures linked to long-term programming [...] Read more.
The rat model of perinatal stress (PRS), in which exposure of pregnant dams to restraint stress reduces maternal behavior, is characterized by a metabolic profile that is reminiscent of the “metabolic syndrome”. We aimed to identify plasma metabolomic signatures linked to long-term programming induced by PRS in aged male rats. This study was conducted in the plasma and frontal cortex. We also investigated the reversal effect of postpartum carbetocin (Cbt) on these signatures, along with its impact on deficits in cognitive, social, and exploratory behavior. We found that PRS induced long-lasting changes in biomarkers of secondary bile acid metabolism in the plasma and glutathione metabolism in the frontal cortex. Cbt treatment demonstrated disease-dependent effects by reversing the metabolite alterations. The metabolomic signatures of PRS were associated with long-term cognitive and emotional alterations alongside endocrinological disturbances. Our findings represent the first evidence of how early life stress may alter the metabolomic profile in aged individuals, thereby increasing vulnerability to CNS disorders. This raises the intriguing prospect that the pharmacological activation of oxytocin receptors soon after delivery through the mother may rectify these alterations. Full article
(This article belongs to the Special Issue Stress-Related Disorders and Depression: From Molecular Basis to Therapy (2nd Edition))
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Review

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22 pages, 1054 KiB  
Review
Bridging Neurobiological Insights and Clinical Biomarkers in Postpartum Depression: A Narrative Review
by Keyi Zhang, Lingxuan He, Zhuoen Li, Ruxuan Ding, Xiaojiao Han, Bingqing Chen, Guoxin Cao, Jiang-Hong Ye, Tian Li and Rao Fu
Int. J. Mol. Sci. 2024, 25(16), 8835; https://doi.org/10.3390/ijms25168835 - 14 Aug 2024
Viewed by 905
Abstract
Postpartum depression (PPD) affects 174 million women worldwide and is characterized by profound sadness, anxiety, irritability, and debilitating fatigue, which disrupt maternal caregiving and the mother–infant relationship. Limited pharmacological interventions are currently available. Our understanding of the neurobiological pathophysiology of PPD remains incomplete, [...] Read more.
Postpartum depression (PPD) affects 174 million women worldwide and is characterized by profound sadness, anxiety, irritability, and debilitating fatigue, which disrupt maternal caregiving and the mother–infant relationship. Limited pharmacological interventions are currently available. Our understanding of the neurobiological pathophysiology of PPD remains incomplete, potentially hindering the development of novel treatment strategies. Recent hypotheses suggest that PPD is driven by a complex interplay of hormonal changes, neurotransmitter imbalances, inflammation, genetic factors, psychosocial stressors, and hypothalamic–pituitary–adrenal (HPA) axis dysregulation. This narrative review examines recent clinical studies on PPD within the past 15 years, emphasizing advancements in neuroimaging findings and blood biomarker detection. Additionally, we summarize recent laboratory work using animal models to mimic PPD, focusing on hormone withdrawal, HPA axis dysfunction, and perinatal stress theories. We also revisit neurobiological results from several brain regions associated with negative emotions, such as the amygdala, prefrontal cortex, hippocampus, and striatum. These insights aim to improve our understanding of PPD’s neurobiological mechanisms, guiding future research for better early detection, prevention, and personalized treatment strategies for women affected by PPD and their families. Full article
(This article belongs to the Special Issue Stress-Related Disorders and Depression: From Molecular Basis to Therapy (2nd Edition))
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18 pages, 1456 KiB  
Review
(R)-(-)-Ketamine: The Promise of a Novel Treatment for Psychiatric and Neurological Disorders
by Hana Shafique, Julie C. Demers, Julia Biesiada, Lalit K. Golani, Rok Cerne, Jodi L. Smith, Marta Szostak and Jeffrey M. Witkin
Int. J. Mol. Sci. 2024, 25(12), 6804; https://doi.org/10.3390/ijms25126804 - 20 Jun 2024
Cited by 3 | Viewed by 1180
Abstract
NMDA receptor antagonists have potential for therapeutics in neurological and psychiatric diseases, including neurodegenerative diseases, epilepsy, traumatic brain injury, substance abuse disorder (SUD), and major depressive disorder (MDD). (S)-ketamine was the first of a novel class of antidepressants, rapid-acting antidepressants, to [...] Read more.
NMDA receptor antagonists have potential for therapeutics in neurological and psychiatric diseases, including neurodegenerative diseases, epilepsy, traumatic brain injury, substance abuse disorder (SUD), and major depressive disorder (MDD). (S)-ketamine was the first of a novel class of antidepressants, rapid-acting antidepressants, to be approved for medical use. The stereoisomer, (R)-ketamine (arketamine), is currently under development for treatment-resistant depression (TRD). The compound has demonstrated efficacy in multiple animal models. Two clinical studies disclosed efficacy in TRD and bipolar depression. A study by the drug sponsor recently failed to reach a priori clinical endpoints but post hoc analysis revealed efficacy. The clinical value of (R)-ketamine is supported by experimental data in humans and rodents, showing that it is less sedating, does not produce marked psychotomimetic or dissociative effects, has less abuse potential than (S)-ketamine, and produces efficacy in animal models of a range of neurological and psychiatric disorders. The mechanisms of action of the antidepressant effects of (R)-ketamine are hypothesized to be due to NMDA receptor antagonism and/or non-NMDA receptor mechanisms. We suggest that further clinical experimentation with (R)-ketamine will create novel and improved medicines for some of the neurological and psychiatric disorders that are underserved by current medications. Full article
(This article belongs to the Special Issue Stress-Related Disorders and Depression: From Molecular Basis to Therapy (2nd Edition))
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