Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Molecular and Cellular Signaling on Antidepressant Mechanisms
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Molecular and Cellular Signaling on Antidepressant Mechanisms

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 (31 August 2021) | Viewed by 23608

Special Issue Editor

Prof. Dr. Akiyoshi Saitoh

E-Mail Website
Guest Editor
Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan
Interests: neuropharmacology; neuropsychopharmacology; opioid; anxiety; depression; reward; fear; antidepressant; anxiolytics; animal model
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Hypotheses on the pathophysiology of depression and mechanisms of antidepressants have greatly changed in recent years. For example, although the classical monoamine hypothesis was revealed to be simplistic, it failed to explain the temporal delay in the therapeutic action of antidepressants. Hence, there remains a clear need to understand the factors associated with the mechanisms underlying antidepressant effects for developing effective, reliable, and safe treatments that have fast action and bring sustained benefits for patients. Recently, several unique mechanisms of neuroplasticity were analyzed in studies of the mechanisms of antidepressants; these range from changes in gene and molecular expression to synaptic plasticity and transmission. Converging lines of evidence have shown that adaptive changes in several of these mechanisms of neuroplasticity are likely to represent the molecular and cellular signaling correlated to therapeutic effects.

The present Special Issue aims to provide an overview of the current research on the promising molecular and cellular signal hypotheses of mechanisms of antidepressants for both standard psychotropic drugs and candidate therapeutic agents for depression that look beyond non-monoaminergic mechanisms.

Prof. Dr. Akiyoshi Saitoh
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

  • antidepressant
  • anxiolytic
  • ketamine
  • opioid
  • cannabinoid
  • depression
  • anxiety
  • fear

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

25 pages, 5521 KiB  
Article
Escitalopram Targets Oxidative Stress, Caspase-3, BDNF and MeCP2 in the Hippocampus and Frontal Cortex of a Rat Model of Depression Induced by Chronic Unpredictable Mild Stress
by Vlad Dionisie, Adela Magdalena Ciobanu, Vlad Alexandru Toma, Mihnea Costin Manea, Ioana Baldea, Diana Olteanu, Alexandra Sevastre-Berghian, Simona Clichici, Mirela Manea, Sorin Riga and Gabriela Adriana Filip
Int. J. Mol. Sci. 2021, 22(14), 7483; https://doi.org/10.3390/ijms22147483 - 13 Jul 2021
Cited by 30 | Viewed by 4784
Abstract
In recent years, escitalopram (ESC) has been suggested to have different mechanisms of action beyond its well known selective serotonin reuptake inhibition. The aim of this study is to investigate the effects of escitalopram on oxidative stress, apoptosis, brain-derived neurotrophic factor (BDNF), Methyl-CpG-binding [...] Read more.
In recent years, escitalopram (ESC) has been suggested to have different mechanisms of action beyond its well known selective serotonin reuptake inhibition. The aim of this study is to investigate the effects of escitalopram on oxidative stress, apoptosis, brain-derived neurotrophic factor (BDNF), Methyl-CpG-binding protein 2 (MeCP2), and oligodendrocytes number in the brain of chronic unpredictable mild stress-induced depressed rats. The animals were randomised in four groups (8 in each group): control, stress, stress + ESC 5 and stress + ESC 5/10. ESC was administered for 42 days in a fixed dose (5 mg/kg b.w.) or in an up-titration regimen (21 days ESC 5 mg/kg b.w. then 21 days ESC 10 mg/kg b.w.). Sucrose preference test (SPT) and elevated plus maze (EPM) were also performed. ESC improved the percentage of sucrose preference, locomotion and anxiety. ESC5/10 reduced the oxidative damage in the hippocampus and improved the antioxidant defence in the hippocampus and frontal lobe. ESC5/10 lowered caspase 3 activity in the hippocampus. Escitalopram had a modulatory effect on BDNF and the number of oligodendrocytes in the hippocampus and frontal lobe and also improved the MeCP2 expressions. The results confirm the multiple pathways implicated in the pathogenesis of depression and suggest that escitalopram exerts an antidepressant effect via different intricate mechanisms. Full article
(This article belongs to the Special Issue Molecular and Cellular Signaling on Antidepressant Mechanisms)
►▼ Show Figures

Graphical abstract

17 pages, 2038 KiB  
Article
2-Phenylethylamine (PEA) Ameliorates Corticosterone-Induced Depression-Like Phenotype via the BDNF/TrkB/CREB Signaling Pathway
by Young-Ju Lee, Hye Ryeong Kim, Chang Youn Lee, Sung-Ae Hyun, Moon Yi Ko, Byoung-Seok Lee, Dae Youn Hwang and Minhan Ka
Int. J. Mol. Sci. 2020, 21(23), 9103; https://doi.org/10.3390/ijms21239103 - 30 Nov 2020
Cited by 40 | Viewed by 5090
Abstract
Depression is a serious medical illness that is one of the most prevalent psychiatric disorders. Corticosterone (CORT) increases depression-like behavior, with some effects on anxiety-like behavior. 2-Phenethylamine (PEA) is a monoamine alkaloid that acts as a central nervous system stimulant in humans. Here, [...] Read more.
Depression is a serious medical illness that is one of the most prevalent psychiatric disorders. Corticosterone (CORT) increases depression-like behavior, with some effects on anxiety-like behavior. 2-Phenethylamine (PEA) is a monoamine alkaloid that acts as a central nervous system stimulant in humans. Here, we show that PEA exerts antidepressant effects by modulating the Brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/cAMP response element binding protein (CREB) signaling pathway in CORT-induced depression. To investigate the potential effects of PEA on CORT-induced depression, we first treated CORT (50 μM)-induced hippocampal neurons with 100 μM PEA for 24 h. We found that treatment with CORT altered dendritic spine architecture; however, treatment with PEA rescued dendritic spine formation via regulation of BDNF/TrkB/CREB signaling. Next, we used a mouse model of CORT-induced depression. Mice were treated with CORT (20 mg/kg) for 21 days, followed by assessments of a battery of depression-like behaviors. During the final four days of CORT exposure, the mice were treated with PEA (50 mg/kg). We found that CORT injection promoted depression-like behavior and significantly decreased BDNF and TrkB expression in the hippocampus. However, treatment with PEA significantly ameliorated the behavioral and biochemical changes induced by CORT. Our findings reveal that PEA exerts antidepressant effects by modulating the BDNF/TrkB/CREB signaling pathway in a mouse model of CORT-induced depression. Full article
(This article belongs to the Special Issue Molecular and Cellular Signaling on Antidepressant Mechanisms)
►▼ Show Figures

Figure 1

Review

Jump to: Research

17 pages, 635 KiB  
Review
Total Recall: Lateral Habenula and Psychedelics in the Study of Depression and Comorbid Brain Disorders
by Matas Vitkauskas and Ajay S. Mathuru
Int. J. Mol. Sci. 2020, 21(18), 6525; https://doi.org/10.3390/ijms21186525 - 7 Sep 2020
Cited by 4 | Viewed by 12762
Abstract
Depression impacts the lives and daily activities of millions globally. Research into the neurobiology of lateral habenula circuitry and the use of psychedelics for treating depressive states has emerged in the last decade as new directions to devise interventional strategies and therapies. Several [...] Read more.
Depression impacts the lives and daily activities of millions globally. Research into the neurobiology of lateral habenula circuitry and the use of psychedelics for treating depressive states has emerged in the last decade as new directions to devise interventional strategies and therapies. Several clinical trials using deep brain stimulation of the habenula, or using ketamine, and psychedelics that target the serotonergic system such as psilocybin are also underway. The promising early results in these fields require cautious optimism as further evidence from experiments conducted in animal systems in ecologically relevant settings, and a larger number of human studies with improved spatiotemporal neuroimaging, accumulates. Designing optimal methods of intervention will also be aided by an improvement in our understanding of the common genetic and molecular factors underlying disorders comorbid with depression, as well as the characterization of psychedelic-induced changes at a molecular level. Advances in the use of cerebral organoids offers a new approach for rapid progress towards these goals. Here, we review developments in these fast-moving areas of research and discuss potential future directions. Full article
(This article belongs to the Special Issue Molecular and Cellular Signaling on Antidepressant Mechanisms)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop