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Advances in the Pharmacology of Monoamines, Histamines and Their Inhibitors

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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: closed (30 June 2023) | Viewed by 8557

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Special Issue Editor

Prof. Dr. Philippe De Deurwaerdère

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Guest Editor

Centre National de la Recherche Scientifique (Unité Mixte de Recherche 5287), CEDEX, 33076 Bordeaux, France
Interests: monoamines; neurochemistry; addiction; Parkinson's disease; schizophrenia; neuropharmacology; mood disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Monoamines and histamines are complex systems participating in the regulation of numerous organs and cells in the central nervous system and periphery. Their level conditions the response of their receptive cells while the targeting of their metabolic pathways remains an important pharmacological endeavor in preclinical and clinical researches. The development of chemical compounds inhibiting the enzymes monoamine oxidases A and B, catechol-O-methyl transferase, and more generally metabolism of monoamines are important strategies in the treatment of neurological diseases such as Alzheimer’s and Parkinson’s disease and neuropsychiatric disease including mood disorders.

The purpose of this Special Issue is to collect research articles and reviews at different levels of analysis dealing with the metabolism of monoamines and histamine and the development of inhibitors or their numerous enzymes and/or transporters. Chemical, molecular, biochemical, and biological studies are welcome in this Special Issue.

Prof. Dr. Philippe De Deurwaerdère
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

chemistry
metabolic pathways
neurodegenerative diseases
aging
monoamine oxidases
tryptophan metabolism
tyrosine metabolism
transporters

Published Papers (3 papers)

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Research

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24 pages, 2250 KiB

Open AccessArticle

Limiting Monoamines Degradation Increases L-DOPA Pro-Locomotor Action in Newborn Rats

by Inès Khsime, Marie Boulain, Abderrahman Fettah, Abdeslam Chagraoui, Gilles Courtand, Philippe De Deurwaerdère, Laurent Juvin and Grégory Barrière

Int. J. Mol. Sci. 2023, 24(19), 14747; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241914747 - 29 Sep 2023

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Abstract

L-DOPA, the precursor of catecholamines, exerts a pro-locomotor action in several vertebrate species, including newborn rats. Here, we tested the hypothesis that decreasing the degradation of monoamines can promote the pro-locomotor action of a low, subthreshold dose of L-DOPA in five-day-old rats. The activity of the degrading pathways involving monoamine oxidases or catechol-O-methyltransferase was impaired by injecting nialamide or tolcapone, respectively. At this early post-natal stage, the capacity of the drugs to trigger locomotion was investigated by monitoring the air-stepping activity expressed by the animals suspended in a harness above the ground. We show that nialamide (100 mg/kg) or tolcapone (100 mg/kg), without effect on their own promotes maximal expression of air-stepping sequences in the presence of a sub-effective dose of L-DOPA (25 mg/kg). Tissue measurements of monoamines (dopamine, noradrenaline, serotonin and some of their metabolites) in the cervical and lumbar spinal cord confirmed the regional efficacy of each inhibitor toward their respective enzyme. Our experiments support the idea that the raise of monoamines boost L-DOPA’s locomotor action. Considering that both inhibitors differently altered the spinal monoamines levels in response to L-DOPA, our data also suggest that maximal locomotor response can be reached with different monoamines environment. Full article

(This article belongs to the Special Issue Advances in the Pharmacology of Monoamines, Histamines and Their Inhibitors)

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18 pages, 6250 KiB

Open AccessArticle

Monoamine Oxidase Inhibitors Prevent Glucose-Dependent Energy Production, Proliferation and Migration of Bladder Carcinoma Cells

by Jessica Resta, Yohan Santin, Mathieu Roumiguié, Elodie Riant, Alexandre Lucas, Bettina Couderc, Claudia Binda, Philippe Lluel, Angelo Parini and Jeanne Mialet-Perez

Int. J. Mol. Sci. 2022, 23(19), 11747; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911747 - 04 Oct 2022

Cited by 4 | Viewed by 1844

Abstract

Bladder cancer is the 10th most common cancer in the world and has a high risk of recurrence and metastasis. In order to sustain high energetic needs, cancer cells undergo complex metabolic adaptations, such as a switch toward aerobic glycolysis, that can be exploited therapeutically. Reactive oxygen species (ROS) act as key regulators of cancer metabolic reprogramming and tumorigenesis, but the sources of ROS remain unidentified. Monoamine oxidases (MAOs) are mitochondrial enzymes that generate H₂O₂ during the breakdown of catecholamines and serotonin. These enzymes are particularly important in neurological disorders, but recently, a new link between MAOs and cancer has been uncovered, involving their production of ROS. At present, the putative role of MAOs in bladder cancer has never been evaluated. We observed that human urothelial tumor explants and the bladder cancer cell line AY27 expressed both MAO-A and MAO-B isoforms. Selective inhibition of MAO-A or MAO-B limited mitochondrial ROS accumulation, cell cycle progression and proliferation of bladder cancer cells, while only MAO-A inhibition prevented cell motility. To test whether ROS contributed to MAO-induced tumorigenesis, we used a mutated form of MAO-A which was unable to produce H₂O₂. Adenoviral transduction of the WT MAO-A stimulated the proliferation and migration of AY27 cells while the Lys305Met MAO-A mutant was inactive. This was consistent with the fact that the antioxidant Trolox strongly impaired proliferation and cell cycle progression. Most interestingly, AY27 cells were highly dependent on glucose metabolism to sustain their growth, and MAO inhibitors potently reduced glycolysis and oxidative phosphorylation, due to pyruvate depletion. Accordingly, MAO inhibitors decreased the expression of proteins involved in glucose transport (GLUT1) and transformation (HK2). In conclusion, urothelial cancer cells are characterized by a metabolic shift toward glucose-dependent metabolism, which is important for cell growth and is under the regulation of MAO-dependent oxidative stress. Full article

(This article belongs to the Special Issue Advances in the Pharmacology of Monoamines, Histamines and Their Inhibitors)

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Review

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29 pages, 2715 KiB

Open AccessReview

Neuroprotective Function of Rasagiline and Selegiline, Inhibitors of Type B Monoamine Oxidase, and Role of Monoamine Oxidases in Synucleinopathies

by Makoto Naoi, Wakako Maruyama and Masayo Shamoto-Nagai

Int. J. Mol. Sci. 2022, 23(19), 11059; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911059 - 21 Sep 2022

Cited by 14 | Viewed by 5373

Abstract

Synucleinopathies are a group of neurodegenerative disorders caused by the accumulation of toxic species of α-synuclein. The common clinical features are chronic progressive decline of motor, cognitive, behavioral, and autonomic functions. They include Parkinson’s disease, dementia with Lewy body, and multiple system atrophy. Their etiology has not been clarified and multiple pathogenic factors include oxidative stress, mitochondrial dysfunction, impaired protein degradation systems, and neuroinflammation. Current available therapy cannot prevent progressive neurodegeneration and “disease-modifying or neuroprotective” therapy has been proposed. This paper presents the molecular mechanisms of neuroprotection by the inhibitors of type B monoamine oxidase, rasagiline and selegiline. They prevent mitochondrial apoptosis, induce anti-apoptotic Bcl-2 protein family, and pro-survival brain- and glial cell line-derived neurotrophic factors. They also prevent toxic oligomerization and aggregation of α-synuclein. Monoamine oxidase is involved in neurodegeneration and neuroprotection, independently of the catalytic activity. Type A monoamine oxidases mediates rasagiline-activated signaling pathways to induce neuroprotective genes in neuronal cells. Multi-targeting propargylamine derivatives have been developed for therapy in various neurodegenerative diseases. Preclinical studies have presented neuroprotection of rasagiline and selegiline, but beneficial effects have been scarcely presented. Strategy to improve clinical trials is discussed to achieve disease-modification in synucleinopathies. Full article

(This article belongs to the Special Issue Advances in the Pharmacology of Monoamines, Histamines and Their Inhibitors)

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