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Molecular Pharmacology of Antidepressants

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

Deadline for manuscript submissions: 20 November 2024 | Viewed by 5898

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Prof. Dr. Anna Tabęcka-Łonczyńska

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Guest Editor

Department of Biotechnology and Cell Biology, Medical College, University of Information Technology and Management in Rzeszow, Sucharskiego 2, 35-225 Rzeszow, Poland
Interests: pharmacology; medical science; neuroscience; cognition; depression; anxiety

Dr. Katarzyna Stachowicz

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Guest Editor

Department of Neurobiology, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343 Kraków, Poland
Interests: cognition; depression; anxiety; DSCAM; GABA; COX-2; mGluRs
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Special Issue Information

Dear Colleagues,

Antidepressants include but are not limited to monoamine oxidase inhibitors, tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin and norepinephrine reuptake inhibitors, and norepinephrine reuptake inhibitors. The FDA approved esketamine for the treatment of drug-resistant depression. The molecular mechanisms of depression and the antidepressant effects of these drugs are still being intensively studied in order to modify them and improve therapeutic effects. In this Special Issue, we invite authors to submit research results that shed new light on drugs already used in the pharmacotherapy of depression and new compounds. Molecular research on the basis of depression will also be welcome, in order to create a compendium of the latest research on depression and its pharmacotherapy.

Prof. Dr. Anna Tabęcka-Łonczyńska
Dr. Katarzyna Stachowicz
Guest Editors

Manuscript Submission Information

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Keywords

depression
pharmacotherapy of depression
molecular mechanisms of depression
mood
pharmacology of depression
antidepressants
drug-drug interactions
in vitro mechanism for antidepressants
side effects of antidepressants

Published Papers (5 papers)

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Research

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23 pages, 2570 KiB

Open AccessArticle

An Innovative Probiotic-Based Supplement to Mitigate Molecular Factors Connected to Depression and Anxiety: An In Vitro Study

by Sara Ferrari, Simone Mulè, Giorgia Rosso, Francesca Parini, Rebecca Galla, Claudio Molinari and Francesca Uberti

Int. J. Mol. Sci. 2024, 25(9), 4774; https://doi.org/10.3390/ijms25094774 - 27 Apr 2024

Viewed by 260

Abstract

The gut–brain axis is a bidirectional relationship between the microbiota and the brain; genes related to the brain and gut synaptic formation are similar. Research on the causal effects of gut microbiota on human behavior, brain development, and function, as well as the underlying molecular processes, has emerged in recent decades. Probiotics have been shown in several trials to help reduce anxiety and depressive symptoms. Because of this, probiotic combinations have been tested in in vitro models to see whether they might modulate the gut and alleviate depression and anxiety. Therefore, we sought to determine whether a novel formulation might affect the pathways controlling anxiety and depression states and alter gut barrier activities in a 3D model without having harmful side effects. Our findings indicate that B. bifidum novaBBF7 10 mg/mL, B. longum novaBLG2 5 mg/mL, and L. paracasei TJB8 10 mg/mL may influence the intestinal barrier and enhance the synthesis of short-chain fatty acids. Additionally, the probiotics studied did not cause neuronal damage and, in combination, exert a protective effect against the condition of anxiety and depression triggered by L-Glutamate. All these findings show that probiotics can affect gut function to alter the pathways underlying anxiety and depression. Full article

(This article belongs to the Special Issue Molecular Pharmacology of Antidepressants)

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13 pages, 2304 KiB

Open AccessArticle

Effects of Anxious Depression on Antidepressant Treatment Response

by Chantal Hampf, Maike Scherf-Clavel, Carolin Weiß, Catherina Klüpfel, Saskia Stonawski, Leif Hommers, Katharina Lichter, Angelika Erhardt-Lehmann, Stefan Unterecker, Katharina Domschke, Sarah Kittel-Schneider, Andreas Menke, Jürgen Deckert and Heike Weber

Int. J. Mol. Sci. 2023, 24(24), 17128; https://doi.org/10.3390/ijms242417128 - 05 Dec 2023

Cited by 1 | Viewed by 876

Abstract

Anxious depression represents a subtype of major depressive disorder and is associated with increased suicidality, severity, chronicity and lower treatment response. Only a few studies have investigated the differences between anxious depressed (aMDD) and non-anxious depressed (naMDD) patients regarding treatment dosage, serum-concentration and drug-specific treatment response. In our naturalistic and prospective study, we investigated whether the effectiveness of therapy including antidepressants (SSRI, SNRI, NaSSA, tricyclics and combinations) in aMDD patients differs significantly from that in naMDD patients. In a sample of 346 patients, we calculated the anxiety somatization factor (ASF) and defined treatment response as a reduction (≥50%) in the Hamilton Depression Rating Scale (HDRS)-21 score after 7 weeks of pharmacological treatment. We did not observe an association between therapy response and the baseline ASF-scores, or differences in therapy outcomes between aMDD and naMDD patients. However, non-responders had higher ASF-scores, and at week 7 aMDD patients displayed a worse therapy outcome than naMDD patients. In subgroup analyses for different antidepressant drugs, venlafaxine-treated aMDD patients showed a significantly worse outcome at week 7. Future prospective, randomized-controlled studies should address the question of a worse therapy outcome in aMDD patients for different psychopharmaceuticals individually. Full article

(This article belongs to the Special Issue Molecular Pharmacology of Antidepressants)

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10 pages, 418 KiB

Open AccessArticle

The Impact of the CYP2D6 and CYP1A2 Gene Polymorphisms on Response to Duloxetine in Patients with Major Depression

by Julian Maciaszek, Tomasz Pawłowski, Tomasz Hadryś, Marta Machowska, Anna Wiela-Hojeńska and Błażej Misiak

Int. J. Mol. Sci. 2023, 24(17), 13459; https://doi.org/10.3390/ijms241713459 - 30 Aug 2023

Viewed by 1594

Abstract

Depression is a global mental health concern, and personalized treatment approaches are needed to optimize its management. This study aimed to investigate the influence of the CYP2D6 and CYP1A2 gene polymorphisms on the efficacy of duloxetine in reducing depressive and anxiety symptoms. A sample of 100 outpatients with major depression, who initiated monotherapy with duloxetine, were followed up. Polymorphisms in the CYP2D6 and CYP1A2 genes were assessed. The severity of depressive and anxiety symptoms was recorded using standardized scales. Adverse drug reactions (ADRs) were analyzed. Statistical analyses, including linear regression, were conducted to examine the relationships between genetic polymorphisms, clinical variables, and treatment outcomes. Patients with higher values of the duloxetine metabolic index (DMI) for CYP2D6, indicating a faster metabolism, achieved a greater reduction in anxiety symptoms. The occurrence of ADRs was associated with a lower reduction in anxiety symptoms. However, no significant associations were found between studied gene polymorphisms and reduction in depressive symptoms. No significant effects of the DMI for CYP1A2 were found. Patients with a slower metabolism may experience less benefit from duloxetine therapy in terms of anxiety symptom reduction. Personalizing treatment based on the CYP2D6 and CYP1A2 gene polymorphisms can enhance the effectiveness of antidepressant therapy and improve patient outcomes. Full article

(This article belongs to the Special Issue Molecular Pharmacology of Antidepressants)

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15 pages, 1921 KiB

Open AccessArticle

Short-Term Irisin Treatment Enhanced Neurotrophin Expression Differently in the Hippocampus and the Prefrontal Cortex of Young Mice

by Manuela Dicarlo, Patrizia Pignataro, Roberta Zerlotin, Clelia Suriano, Chiara Zecca, Maria Teresa Dell’Abate, Giuseppina Storlino, Angela Oranger, Lorenzo Sanesi, Giorgio Mori, Maria Grano, Graziana Colaianni and Silvia Colucci

Int. J. Mol. Sci. 2023, 24(11), 9111; https://doi.org/10.3390/ijms24119111 - 23 May 2023

Cited by 2 | Viewed by 1377

Abstract

As a result of physical exercise, muscle releases multiple exerkines, such as “irisin”, which is thought to induce pro-cognitive and antidepressant effects. We recently demonstrated in young healthy mice the mitigation of depressive behaviors induced by consecutive 5 day irisin administration. To understand which molecular mechanisms might be involved in such effect, we here studied, in a group of mice previously submitted to a behavioral test of depression, the gene expression of neurotrophins and cytokines in the hippocampus and prefrontal cortex (PFC), two brain areas frequently investigated in the depression pathogenesis. We found significantly increased mRNA levels of nerve growth factor (NGF) and fibroblast growth factor 2 (FGF-2) in the hippocampus and brain-derived growth factor (BDNF) in the PFC. We did not detect a difference in the mRNA levels of interleukin 6 (IL-6) and IL-1β in both brain regions. Except for BDNF in the PFC, two-way ANOVA analysis did not reveal sex differences in the expression of the tested genes. Overall, our data evidenced a site-specific cerebral modulation of neurotrophins induced by irisin treatment in the hippocampus and the PFC, contributing to the search for new antidepressant treatments targeted at single depressive events with short-term protocols. Full article

(This article belongs to the Special Issue Molecular Pharmacology of Antidepressants)

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Review

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22 pages, 1238 KiB

Open AccessReview

Molecular Mechanisms of Reelin in the Enteric Nervous System and the Microbiota–Gut–Brain Axis: Implications for Depression and Antidepressant Therapy

by Ciara S. Halvorson, Carla Liria Sánchez-Lafuente, Jenessa N. Johnston, Lisa E. Kalynchuk and Hector J. Caruncho

Int. J. Mol. Sci. 2024, 25(2), 814; https://doi.org/10.3390/ijms25020814 - 09 Jan 2024

Viewed by 1190

Abstract

Current pharmacological treatments for depression fail to produce adequate remission in a significant proportion of patients. Increasingly, other systems, such as the microbiome–gut–brain axis, are being looked at as putative novel avenues for depression treatment. Dysbiosis and dysregulation along this axis are highly comorbid with the severity of depression symptoms. The endogenous extracellular matrix protein reelin is present in all intestinal layers as well as in myenteric and submucosal ganglia, and its receptors are also present in the gut. Reelin secretion from subepithelial myofibroblasts regulates cellular migration along the crypt–villus axis in the small intestine and colon. Reelin brain expression is downregulated in mood and psychotic disorders, and reelin injections have fast antidepressant-like effects in animal models of depression. This review seeks to discuss the roles of reelin in the gastrointestinal system and propose a putative role for reelin actions in the microbiota–gut–brain axis in the pathogenesis and treatment of depression, primarily reflecting on alterations in gut epithelial cell renewal and in the clustering of serotonin transporters. Full article

(This article belongs to the Special Issue Molecular Pharmacology of Antidepressants)

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