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Molecular Crosstalk in Stress-Induced Psychopathology
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Molecular Crosstalk in Stress-Induced Psychopathology

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 June 2026 | Viewed by 1078

Special Issue Editors

Dr. Ilaria Demori

E-Mail Website
Guest Editor
Department of Pharmacy (DIFAR), University of Genova, Viale Benedetto XV 3, 16132 Genova, Italy
Interests: psychoneuroendocrineimmunology; psychopathology; stress; fibromyalgia; nutrition
Prof. Dr. Natalia V. Gulyaeva

E-Mail Website
Guest Editor
1. Laboratory of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, 117485 Moscow, Russia
2. Research and Clinical Center for Neuropsychiatry of Moscow Healthcare Department, 115419 Moscow, Russia
Interests: adaptation; Alzheimer animal models; apoptosis; behaviour; biomarkers; cellular models; cerebral ischemia; dementia; depression; epilepsy; excitotoxicity; free radicals; glia; glucocorticoid signalin
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Since the pioneering work of Hans Selye, the human stress response has been recognized as an adaptive mechanism essential for survival. Nonetheless, mounting evidence indicates that early-life adversity and chronic psychosocial stress represent significant risk factors for the onset of various mental disorders, including depression, anxiety, eating disorders, substance abuse and neurodegenerative diseases, e.g., Alzheimer’s and Parkinson’s disease. The framework of psychoneuroendocrineimmunology (PNEI) offers a comprehensive network-based model to interpret the intricate bidirectional communication among key biological systems. This includes interactions between hormones, neurotransmitters, cytokines, across the blood-brain barrier and microbiota-derived metabolites, all of which are modulated by stress and may contribute to psychopathological outcomes.

The primary objective of this Special Issue is to advance current understanding of the molecular mechanisms underlying these complex inter-system interactions in the pathogenesis of mental disorders and brain pathology. We welcome contributions focused on molecular-level investigations, including preclinical studies, clinical trials, intervention research, narrative, or systematic reviews, as well as theoretical mathematical models of interactions.

Dr. Ilaria Demori
Prof. Dr. Natalia V. Gulyaeva
Guest Editors

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Keywords

  • Depression
  • Anxiety
  • Post-traumatic stress disorder
  • Early life stress
  • Microbiota–gut–brain axis
  • Blood–brain barrier
  • Neurotransmission
  • Neuroinflammation
  • Eating disorders
  • Addiction
  • Psychoneuroendocrineimmunology
  • Allostasis

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Published Papers (1 paper)

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Research

21 pages, 2483 KB  
Article
Glucocorticoid Signaling-Associated Gene Expression in the Hippocampus and Frontal Cortex of Chronically Isolated Normotensive and Hypertensive Rats and the Responsiveness to Acute Restraint Stress
by Alexey Kvichansky, Liya Tretyakova, Yulia Moiseeva, Viktoriia Ovchinnikova, Diana Mamedova, Olga Nedogreeva, Natalia Lazareva, Natalia Gulyaeva and Mikhail Stepanichev
Int. J. Mol. Sci. 2025, 26(24), 12050; https://doi.org/10.3390/ijms262412050 - 15 Dec 2025
Viewed by 778
Abstract
Genotypic characteristics may determine the body’s response to stressful conditions as well as its susceptibility to cardiovascular diseases and stroke. Old age worsens the course of these diseases, and often concomitant hypertension can negatively affect brain function, especially in cases of social isolation. [...] Read more.
Genotypic characteristics may determine the body’s response to stressful conditions as well as its susceptibility to cardiovascular diseases and stroke. Old age worsens the course of these diseases, and often concomitant hypertension can negatively affect brain function, especially in cases of social isolation. In this work, we studied how social isolation and hypertension affect the transcription activity of genes associated with glucocorticoid signaling in the rat brain. The study was performed on 10-month-old rats of the outbred Wistar stock (n = 48) and the inbred spontaneously hypertensive (SHR) strain (n = 28). The animals of each genotype were divided into groups, one of which was kept in home cages in groups of 3–4 individuals, and the other in single cages for 3 months. Physiological parameters and plasma corticosterone were controlled before the start and after 3 months of isolation. Each group was additionally divided into two subgroups: one subjected to 1 h of restraint stress, and changes in blood glucose and corticosterone levels were assessed. At the end, the levels of Nr3c1, Nr3c2, Hsd11b1, and Fkbp5 mRNAs were measured in the hippocampus and frontal cortex using the Q-PCR technique. After isolation, weight gain stopped in SHRs, although blood pressure did not change, and heart rate increased in rats of both genotypes. In response to restraint, there was practically no increase in corticosterone in isolated Wistar rats, whereas in SHRs, there were significant glucose and corticosterone responses. Significant disruptions in the system responsible for corticosterone-activated signaling cascades were found in the brains of SHR rats. The transcriptional activity of genes encoding corticosterone receptors and proteins regulating their action was reduced in the hippocampus and frontal cortex in SHRs compared to Wistar rats. However, neither isolation nor acute stress significantly affected the contents of transcripts studied. Meanwhile, after isolation, the relationships between the expression of these genes changed significantly, in different directions, in rats of the studied genotypes, both within and between brain structures. Thus, the SHR genotype is associated with persistent changes in the brain that affect the expression of glucocorticoid-associated genes. This indicates a more complex regulation of the stress response, not limited only by the feedback system within the hypothalamic–pituitary–adrenocortical or sympatho-adrenomedullary systems, but operated at the level of the limbic system and the cerebral cortex. Full article
(This article belongs to the Special Issue Molecular Crosstalk in Stress-Induced Psychopathology)
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