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Biomedicines
Special Issues
Neurotransmitters in Health and Diseases
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Neurotransmitters in Health and Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 2962

Special Issue Editors

Dr. Zsolt Bagosi

E-Mail Website
Guest Editor
Szegedi Tudományegyetem (SZTE), Szeged, Hungary
Interests: neurotransmitter; dopamine; addiction research
Dr. Krisztina Csabafi

E-Mail Website
Guest Editor
Department of Pathophysiology, University of Szeged Faculty of Medicine, Szeged, Hungary
Interests: neuropeptides; central nervous system

Special Issue Information

Dear Colleagues,

Neurotransmitters are chemical messengers that convey chemical signals from one neuron to another cell, such as a nerve cell, muscle cell or gland. Structurally, neurotransmitters are tyopically amino acids, monoamines or peptides, and they can be functionally classified into inhibitory, such as GABA and dopamine, and excitatory, such as glutamate and acetylcholine; however, they can also be classified into neurohormones, including corticotropin-releasing factor, arginine vasopressin and oxytocin, and neuromodulators, including noradrenaline, serotonin and histamine. Under physiological conditions, neurotransmitters modulate endocrine, autonomic and behavioral processes to maintain the homeostasis of the body, but their dysbalance may contribute to the pathogenesis of psychiatric disorders, such as anxiety, depression and substance use disorder, or neurological diseases, such as Alzheimers’s, Parkinson’s and Huntington’s disease. In this Special Issue of Biomedicines, I would like to invite you to share your recent research in the form of a review or original article addressing the role of neurotransmitters in health and disease.

Dr. Zsolt Bagosi
Dr. Krisztina Csabafi
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • neurotransmitters
  • GABA
  • dopamine
  • glutamate
  • acetylcholine
  • neurohormones
  • neuromodulators

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Published Papers (3 papers)

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Research

15 pages, 2844 KiB  
Article
Changes in Locomotor Activity Observed During Acute Nicotine Withdrawal Can Be Attenuated by Ghrelin and GHRP-6 in Rats
by Jázmin Ayman, András Buzás, Roberta Dochnal, Miklós Palotai, Miklós Jászberényi and Zsolt Bagosi
Biomedicines 2025, 13(1), 143; https://doi.org/10.3390/biomedicines13010143 - 9 Jan 2025
Viewed by 765
Abstract
Background/Objectives: Ghrelin and growth hormone-releasing peptide 6 (GHRP-6) are peptides which can stimulate GH release, acting through the same receptor. Ghrelin and its receptor have been involved in reward sensation and addiction induced by natural and artificial drugs, including nicotine. The present study [...] Read more.
Background/Objectives: Ghrelin and growth hormone-releasing peptide 6 (GHRP-6) are peptides which can stimulate GH release, acting through the same receptor. Ghrelin and its receptor have been involved in reward sensation and addiction induced by natural and artificial drugs, including nicotine. The present study aimed to investigate the impacts of ghrelin and GHRP-6 on the horizontal and vertical activity in rats exposed to chronic nicotine treatment followed by acute nicotine withdrawal. Methods: Male and female Wistar rats were exposed daily to intraperitoneal (ip) injection with 2 mg/kg nicotine or saline solution for 7 days, twice a day (at 8:00 and at 20:00). In parallel, the rats were exposed daily to an intracerebroventricular (icv) injection with 1 μg/2 μL ghrelin or 1 μg/2 μL GHRP-6 or saline solution for 7 days, once a day (at 8:00). On the morning of the eighth day (12 h after the last ip administration) and the ninth day (24 h after the last ip administration), the horizontal and vertical activity were monitored in a conducta system. Results: On the eighth day, in nicotine-treated rats a significant hyperactivity was observed, that was reduced significantly by ghrelin and GHRP-6. On the ninth day, in nicotine-treated rats a significant hypoactivity was assessed that was reversed significantly by ghrelin and GHRP-6. Conclusions: Based on the present results, the changes in horizontal and vertical activity observed after 12 and 24 h of nicotine withdrawal can be attenuated by ghrelin and GHRP-6. Full article
(This article belongs to the Special Issue Neurotransmitters in Health and Diseases)
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19 pages, 3755 KiB  
Article
Angiotensin IV Receptors in the Rat Prefrontal Cortex: Neuronal Expression and NMDA Inhibition
by Zsolt Tamás Papp, Polett Ribiczey, Erzsébet Kató, Zsuzsanna E. Tóth, Zoltán V. Varga, Zoltán Giricz, Adrienn Hanuska, Mahmoud Al-Khrasani, Ákos Zsembery, Tibor Zelles, Laszlo G. Harsing, Jr. and László Köles
Biomedicines 2025, 13(1), 71; https://doi.org/10.3390/biomedicines13010071 - 31 Dec 2024
Cited by 1 | Viewed by 816
Abstract
Background: N-methyl-D-aspartate type glutamate receptors (NMDARs) are fundamental to neuronal physiology and pathophysiology. The prefrontal cortex (PFC), a key region for cognitive function, is heavily implicated in neuropsychiatric disorders, positioning the modulation of its glutamatergic neurotransmission as a promising therapeutic target. Our recently [...] Read more.
Background: N-methyl-D-aspartate type glutamate receptors (NMDARs) are fundamental to neuronal physiology and pathophysiology. The prefrontal cortex (PFC), a key region for cognitive function, is heavily implicated in neuropsychiatric disorders, positioning the modulation of its glutamatergic neurotransmission as a promising therapeutic target. Our recently published findings indicate that AT1 receptor activation enhances NMDAR activity in layer V pyramidal neurons of the rat PFC. At the same time, it suggests that alternative angiotensin pathways, presumably involving AT4 receptors (AT4Rs), might exert inhibitory effects. Angiotensin IV (Ang IV) and its analogs have demonstrated cognitive benefits in animal models of learning and memory deficits. Methods: Immunohistochemistry and whole-cell patch-clamp techniques were used to map the cell-type-specific localization of AT4R, identical to insulin-regulated aminopeptidase (IRAP), and to investigate the modulatory effects of Ang IV on NMDAR function in layer V pyramidal cells of the rat PFC. Results: AT4R/IRAP expression was detected in pyramidal cells and GABAergic interneurons, but not in microglia or astrocytes, in layer V of the PFC in 9–12-day-old and 6-month-old rats. NMDA (30 μM) induced stable inward cation currents, significantly inhibited by Ang IV (1 nM–1 µM) in a subset of pyramidal neurons. This inhibition was reproduced by the IRAP inhibitor LVVYP-H7 (10–100 nM). Synaptic isolation of pyramidal neurons did not affect the Ang IV-mediated inhibition of NMDA currents. Conclusions: Ang IV/IRAP-mediated inhibition of NMDA currents in layer V pyramidal neurons of the PFC may represent a way of regulating cognitive functions and thus a potential pharmacological target for cognitive impairments and related neuropsychiatric disorders. Full article
(This article belongs to the Special Issue Neurotransmitters in Health and Diseases)
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11 pages, 4376 KiB  
Article
Monosodium Glutamate Treatment Elevates the Immunoreactivity of GFAP and S100β in Caudate Nucleus of the Striatum in Rats
by Karol Rycerz, Aleksandra Krawczyk, Jadwiga Jaworska-Adamu and Marcin B. Arciszewski
Biomedicines 2024, 12(12), 2763; https://doi.org/10.3390/biomedicines12122763 - 4 Dec 2024
Viewed by 809
Abstract
Background Monosodium glutamate (MSG) in its anionic form, glutamate, is one of the main excitatory amino acids. Excess of this neurotransmitter may lead to excitotoxicity affecting neurons and astrocytes responsible for glutamate metabolism in different brain areas of animals. The aim of the [...] Read more.
Background Monosodium glutamate (MSG) in its anionic form, glutamate, is one of the main excitatory amino acids. Excess of this neurotransmitter may lead to excitotoxicity affecting neurons and astrocytes responsible for glutamate metabolism in different brain areas of animals. The aim of the study was to investigate the immunoreactivity of glial fibrillary acidic protein (GFAP) and S100β protein in the caudate nucleus of rats under the condition of elevated glutamate levels. Methods: Fifteen rats were divided into a control group receiving saline and MSG2 and MSG4 groups receiving 2 g/kg b.w. MSG and 4 g/kg b.w. MSG, respectively, for 3 days. An immunohistochemical reaction was conducted on frontal sections containing the caudate nucleus with use of antibodies against GFAP and S100β. Results: Analyses indicated elevated density of astrocytes immunoreactive for the studied proteins in the caudate nucleus in animals receiving MSG. The studied glial cells also demonstrated increased immunostaining intensity for both GFAP and S100β immunoreactive cells especially in the MSG4 group. The number of GFAP-positive processes in astrocytes was similar in all studied groups. Conclusions: The studies demonstrate a potential response of astrocytes to the effect of MSG administration in the caudate nucleus. It was shown that GFAP- and S100β-positive astrocytes in the caudate nucleus may act differently, suggesting distinct roles of these proteins against glutamate excitotoxicity. Full article
(This article belongs to the Special Issue Neurotransmitters in Health and Diseases)
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