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Novel Pharmacological Strategies Based on Genetic and Neurobiological Pathways of Depression

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: closed (28 February 2023) | Viewed by 6133

Special Issue Editor

Prof. Dr. Sergei B. Seredenin

E-Mail Website
Guest Editor
Federal State Budgetary Institution «Research Zakusov Institute of Pharmacology», Moscow, Russia
Interests: depression; neuropsychopharmacology; anxiolytics; neurodegenerative diseases; pharmacogenetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Depression is one of the most common mental health disorders and a significant worldwide medical and social problem. Multiple basic and clinical studies indicate the complexity and multifactorial nature of depression that is determined by the interactions of a wide range of social, psychological, hereditary, and epigenetic factors. In recent decades, significant progress has been achieved in uncovering the molecular neurobiology of depression, and as a result, several effective and safe antidepressants have emerged to cure this challenging disease. However, understanding of factors underlying heterogeneity depression pathogenesis and phenotypes, including individual variability in treatment response to antidepressants and side effect manifestation, requires strengthening efforts for the search and development of novel medicines directed at diverse mechanisms and associated targets to personalize the therapy of depression and related disorders.

This Special Issue encourages authors to contribute original research or review papers highlighting recent advances in the neurobiology of depression and leading approaches to the treatment of this disease with the focus on the disturbances of monoaminergic, glutamatergic, endocannabinoid, and GABAergic neurotransmission, dysfunctions of the hypothalamic–pituitary–adrenal system, deficiency of neurotrophins and endogenous neurosteroids, activation of neuroinflammation, involvement of chaperones, cellular stress mechanisms, synaptic alterations, and genetic and epigenetic factors.

Prof. Dr. Sergei B. Seredenin
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. 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

  • depression
  • neuroinflammation
  • genetic factors
  • COVID-19-associated depression
  • pharmacotherapy
  • sigma-1R
  • animal models
  • neuroplasticity
  • epigenetics

Published Papers (2 papers)

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Research

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23 pages, 5945 KiB  
Article
Effects of Tail Pinch on BDNF and trkB Expression in the Hippocampus of Roman Low- (RLA) and High-Avoidance (RHA) Rats
by Maria Pina Serra, Francesco Sanna, Marianna Boi, Marcello Trucas, Alberto Fernández-Teruel, Maria Giuseppa Corda, Osvaldo Giorgi and Marina Quartu
Int. J. Mol. Sci. 2023, 24(11), 9498; https://doi.org/10.3390/ijms24119498 - 30 May 2023
Cited by 1 | Viewed by 1167
Abstract
In this article, we describe the effects of tail pinch (TP), a mild acute stressor, on the levels of brain-derived neurotrophic factor (BDNF) and its tyrosine kinase receptor B (trkB) proteins in the hippocampus (HC) of the outbred Roman High- (RHA) and Low-Avoidance [...] Read more.
In this article, we describe the effects of tail pinch (TP), a mild acute stressor, on the levels of brain-derived neurotrophic factor (BDNF) and its tyrosine kinase receptor B (trkB) proteins in the hippocampus (HC) of the outbred Roman High- (RHA) and Low-Avoidance (RLA) rats, one of the most validated genetic models for the study of fear/anxiety- and stress-related behaviors. Using Western blot (WB) and immunohistochemistry assays, we show for the first time that TP induces distinct changes in the levels of BDNF and trkB proteins in the dorsal (dHC) and ventral (vHC) HC of RHA and RLA rats. The WB assays showed that TP increases BDNF and trkB levels in the dHC of both lines but induces opposite changes in the vHC, decreasing BDNF levels in RHA rats and trkB levels in RLA rats. These results suggest that TP may enhance plastic events in the dHC and hinder them in the vHC. Immunohistochemical assays, carried out in parallel to assess the location of changes revealed by the WB, showed that, in the dHC, TP increases BDNF-like immunoreactivity (LI) in the CA2 sector of the Ammon’s horn of both Roman lines and in the CA3 sector of the Ammon’s horn of RLA rats while, in the dentate gyrus (DG), TP increases trkB-LI in RHA rats. In contrast, in the vHC, TP elicits only a few changes, represented by decreases of BDNF- and trkB-LI in the CA1 sector of the Ammon’s horn of RHA rats. These results support the view that the genotypic/phenotypic features of the experimental subjects influence the effects of an acute stressor, even as mild as TP, on the basal BDNF/trkB signaling, leading to different changes in the dorsal and ventral subdivisions of the HC. Full article
(This article belongs to the Special Issue Novel Pharmacological Strategies Based on Genetic and Neurobiological Pathways of Depression)
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Review

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45 pages, 2978 KiB  
Review
The Melanocortin System: A Promising Target for the Development of New Antidepressant Drugs
by Dmitrii D. Markov, Oleg V. Dolotov and Igor A. Grivennikov
Int. J. Mol. Sci. 2023, 24(7), 6664; https://doi.org/10.3390/ijms24076664 - 3 Apr 2023
Cited by 2 | Viewed by 4611
Abstract
Major depression is one of the most prevalent mental disorders, causing significant human suffering and socioeconomic loss. Since conventional antidepressants are not sufficiently effective, there is an urgent need to develop new antidepressant medications. Despite marked advances in the neurobiology of depression, the [...] Read more.
Major depression is one of the most prevalent mental disorders, causing significant human suffering and socioeconomic loss. Since conventional antidepressants are not sufficiently effective, there is an urgent need to develop new antidepressant medications. Despite marked advances in the neurobiology of depression, the etiology and pathophysiology of this disease remain poorly understood. Classical and newer hypotheses of depression suggest that an imbalance of brain monoamines, dysregulation of the hypothalamic-pituitary-adrenal axis (HPAA) and immune system, or impaired hippocampal neurogenesis and neurotrophic factors pathways are cause of depression. It is assumed that conventional antidepressants improve these closely related disturbances. The purpose of this review was to discuss the possibility of affecting these disturbances by targeting the melanocortin system, which includes adrenocorticotropic hormone-activated receptors and their peptide ligands (melanocortins). The melanocortin system is involved in the regulation of various processes in the brain and periphery. Melanocortins, including peripherally administered non-corticotropic agonists, regulate HPAA activity, exhibit anti-inflammatory effects, stimulate the levels of neurotrophic factors, and enhance hippocampal neurogenesis and neurotransmission. Therefore, endogenous melanocortins and their analogs are able to complexly affect the functioning of those body’s systems that are closely related to depression and the effects of antidepressants, thereby demonstrating a promising antidepressant potential. Full article
(This article belongs to the Special Issue Novel Pharmacological Strategies Based on Genetic and Neurobiological Pathways of Depression)
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