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Biomedicines
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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 2438

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

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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 564
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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Figure 1

Figure 1
<p>The actions of nicotine and mecamylamine on the brain. During smoking, nicotine reaches the brain and activates the nicotinergic acetylcholine receptor (nAchR) in the ventral tegmental area (VTA) and substantia nigra (SN), stimulating the release of dopamine in the nucleus accumbens (NAcc) and caudate–putamen (CP). Mecamylamine can inhibit the nAchR and precipitate the symptoms of nicotine withdrawal.</p> Full article ">Figure 2
<p>The actions of ghrelin and GHRP-6 on the brain. During hunger, ghrelin reaches the brain and activates the ghrelin receptor (GHSR1a) in the hypothalamus. In the hypothalamus, it activates the orexigenic mediators, neuropeptide Y (NPY) and agouti-related peptide (AgRP), expressed in the nucleus arcuatus (Arc), and consequently, the orexigenic regulators, orexin and melanin-concentrating hormone (MCH), expressed in the lateral hypothalamus, leading to increased food intake and body weight. Growth hormone-releasing peptide 6 (GHRP-6) is considered an antagonist of the GHSR1a, although it can act as an agonist stimulating the GH release and mimicking the orexigenic effects of ghrelin.</p> Full article ">Figure 3
<p>The horizontal activity determined on the 8th day in rats exposed to 7 days of nicotine treatment. Values are presented as means ± SEM. The numbers in parentheses represent the number of animals in each group. A statistically significant difference was accepted for <span class="html-italic">p</span> &lt; 0.05 and indicated with * for nicotine ip + saline icv vs. saline ip + saline icv and with # for nicotine ip + ghrelin or GHRP-6 icv vs. nicotine ip + saline icv.</p> Full article ">Figure 4
<p>The vertical activity determined on the 8th day in rats exposed to 7 days of nicotine treatment. Values are presented as means ± SEM. The numbers in parentheses represent the number of animals in each group. A statistically significant difference was accepted for <span class="html-italic">p</span> &lt; 0.05 and indicated with * for nicotine ip + saline icv vs. saline ip + saline icv and with # for nicotine ip + ghrelin or GHRP-6 icv vs. nicotine ip + saline icv.</p> Full article ">Figure 5
<p>The horizontal activity determined on the 9th day in rats exposed to 7 days of nicotine treatment and 1 day of withdrawal. Values are presented as means ± SEM. The numbers in parentheses represent the number of animals in each group. A statistically significant difference was accepted for <span class="html-italic">p</span> &lt; 0.05 and indicated with * for nicotine ip + saline icv vs. saline ip + saline icv and with # for nicotine ip + ghrelin or GHRP-6 icv vs. nicotine ip + saline icv.</p> Full article ">Figure 6
<p>The vertical activity determined on the 9th day in rats exposed to 7 days of nicotine treatment and 1 day of withdrawal. Values are presented as means ± SEM. The numbers in parentheses represent the number of animals in each group. A statistically significant difference was accepted for <span class="html-italic">p</span> &lt; 0.05 and indicated with * for nicotine ip + saline icv vs. saline ip + saline icv and with # for nicotine ip + ghrelin or GHRP-6 icv vs. nicotine ip + saline icv.</p> Full article ">Figure 7
<p>The interaction of ghrelin and nicotine in the brain. Chronic nicotine treatment is associated with general hyperactivity, whereas acute nicotine withdrawal with general hypoactivity can be attenuated by ghrelin and growth hormone-releasing peptide 6 (GHRP-6). Both ghrelin and nicotine can stimulate the dopamine release in the striatum, represented by nucleus accumbens (NAcc) and caudate–putamen (CP). The interaction between nicotine and ghrelin is most probably mediated by the cholinergic–dopaminergic reward link, which encompasses the afferent cholinergic projection from the laterodorsal tegmentum (LDT) to the ventral tegmental area (VTA), and the mesolimbic dopaminergic pathway that emerges from the dopaminergic neurons situated in the VTA and ends in the NAcc.</p> Full article ">
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
Viewed by 647
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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Figure 1

Figure 1
<p>Inhibitory effect of Ang II on NMDA-induced currents in layer V pyramidal neurons of the medial prefrontal cortex in 9–12-day-old rats. Whole-cell patch-clamp recordings were performed at a holding potential of −70 mV. NMDA (30 µM) in aCSF was applied three times (T<sub>1</sub>, T<sub>2</sub>, T<sub>3</sub>) for 1.5 min, with 10 min intervals between applications. Ang II (3 μM) was superfused for 5 min before and during T<sub>3</sub>. (<b>A</b>) Inhibitory effects of Ang IV on the NMDA current at T<sub>3</sub> are expressed as the percentage inhibition of the response measured at T<sub>2</sub>. Data are presented as mean ± SEM. Red columns represent the percentage inhibition of NMDA-induced current responses (T<sub>3</sub>/T<sub>2</sub>) in cells where Ang II inhibited NMDA receptor-mediated ion currents. The number of responsive cells out of the total number of cells tested is shown in the red columns. * <span class="html-italic">p</span> &lt; 0.01, indicating a significant difference from controls. (<b>B</b>) Representative tracing of a current response to 30 μM NMDA at T<sub>2</sub> and T<sub>3</sub>, in the presence of 3 μM Ang II superfused for 5 min before and during T<sub>3</sub>.</p> Full article ">Figure 2
<p>Protein expression of IRAP (green) in distinct layers of the medial prefrontal cortex in young (10-day-old) (<b>A</b>) and adult (6-month-old) (<b>B</b>) rats. The receptor is highly expressed in the cells of layers II–III and V–VI at both ages. DAPI (blue) was used as a counterstain. Scale bars: 200 μm (left panels in (<b>A</b>,<b>B</b>)) and 50 μm (right panels in (<b>A</b>,<b>B</b>)).</p> Full article ">Figure 3
<p>Representative images of the immunofluorescent detection of IRAP in distinct cell types in layer V of the mPFC in (<b>A</b>) young (10-day-old) and (<b>B</b>) adult (6-month-old) rats. The receptor is highly expressed in cells with a pyramidal morphology (green arrows) and in GABAergic interneurons (yellow arrows) but not in microglia or astrocytes (red arrows). GAD67, IBA1, and GFAP were used as markers. DAPI was used as a counterstain (blue). Notably, IRAP staining is weaker in 10-day-old animals compared to 6-month-old rats. Furthermore, this reduction is particularly pronounced in GABAergic interneurons but to a lesser extent in pyramidal cells in the 10-day-old rats. Scale bar: 50 μm.</p> Full article ">Figure 3 Cont.
<p>Representative images of the immunofluorescent detection of IRAP in distinct cell types in layer V of the mPFC in (<b>A</b>) young (10-day-old) and (<b>B</b>) adult (6-month-old) rats. The receptor is highly expressed in cells with a pyramidal morphology (green arrows) and in GABAergic interneurons (yellow arrows) but not in microglia or astrocytes (red arrows). GAD67, IBA1, and GFAP were used as markers. DAPI was used as a counterstain (blue). Notably, IRAP staining is weaker in 10-day-old animals compared to 6-month-old rats. Furthermore, this reduction is particularly pronounced in GABAergic interneurons but to a lesser extent in pyramidal cells in the 10-day-old rats. Scale bar: 50 μm.</p> Full article ">Figure 4
<p>Inhibitory effects of Ang IV on the NMDA-induced current in layer V pyramidal neurons of the mPFC in young (9–12 days old) rats. Whole-cell patch-clamp recordings were performed at a holding potential of −70 mV. NMDA (30 µM) in aCSF was applied three times for 1.5 min (T<sub>1</sub>, T<sub>2</sub>, T<sub>3</sub>), with a 10 min interval between applications. Ang IV (1 nM to 1 μM) was superfused 5 min before and during T<sub>3</sub>. (<b>A</b>) Inhibitory effects of Ang IV on the NMDA current at T<sub>3</sub> are expressed as the percentage inhibition of the response measured at T<sub>2</sub>. Data are presented as mean ± SEM. Red columns represent the percentage inhibition of NMDA-induced current responses in cells where Ang IV inhibited NMDA receptor-mediated ion currents. The number of responsive cells out of the total number of cells tested is indicated in the red columns. * <span class="html-italic">p</span> &lt; 0.01; significant difference from controls. (<b>B</b>) Representative tracing of a current response to 30 μM NMDA after T<sub>2</sub> and T<sub>3</sub> and in the presence of Ang IV (100 nM) for 5 min before and during T<sub>3</sub>.</p> Full article ">Figure 5
<p>The inhibitory effect of Ang IV persisted during synaptic isolation by a Ca<sup>2</sup>⁺-free solution or TTX-containing aCSF on the NMDA-induced current in layer V pyramidal neurons of the mPFC in young (9–12 day-old) rats. Whole-cell patch-clamp recordings were performed at a holding potential of −70 mV. NMDA (30 µM) was applied three times for 1.5 min (T<sub>1</sub>, T<sub>2</sub>, T<sub>3</sub>), with a 10 min interval between applications. Ang IV (100 nM) was superfused 5 min before and during T<sub>3</sub>, while the Ca<sup>2</sup>⁺-free solution or TTX (0.5 μM) was superfused throughout the experiment. The inhibitory effects of Ang IV on the NMDA current at T<sub>3</sub> are expressed as the percentage inhibition of the response measured at T<sub>2</sub>. Data are presented as mean ± SEM. Red columns represent the percentage inhibition of NMDA-induced current responses in cells where Ang IV inhibited NMDA receptor-mediated ion currents. The number of responsive cells out of the total number of cells tested is indicated in the red columns. * <span class="html-italic">p</span> &lt; 0.01; significant difference from controls.</p> Full article ">Figure 6
<p>The inhibitory effect of Ang IV was reproduced by the IRAP inhibitor LVVYP-H7 on the NMDA-induced current in layer V pyramidal neurons of the mPFC in young (9–12 days old) rats. Whole-cell patch-clamp recordings were performed at a holding potential of −70 mV. NMDA (30 µM) in aCSF was applied three times for 1.5 min (T<sub>1</sub>, T<sub>2</sub>, T<sub>3</sub>), with a 10 min interval between applications. LVVYP-H7 (1 nM–100 nM) was superfused for 5 min before and during T<sub>3</sub>. The inhibitory effects of LVVYP-H7 on the NMDA current at T<sub>3</sub> are expressed as the percentage inhibition of the response measured at T2. Data are presented as mean ± SEM. Red columns represent the percentage inhibition of NMDA-induced current responses in cells where LVVYP-H7 inhibited NMDA receptor-mediated ion currents. The number of responsive cells out of the total number of cells tested is indicated in the red columns. * <span class="html-italic">p</span> &lt; 0.01, indicating a significant difference from the control.</p> Full article ">
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 699
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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Figure 1

Figure 1
<p>Immunohistochemical staining of caudate nucleus area using anti-GFAP antibody in Control group (<b>A</b>), MSG2 group (<b>B</b>), MSG4 group (<b>C</b>) and anti-S100β antibody in Control group (<b>D</b>), MSG2 group (<b>E</b>) and MSG4 group (<b>F</b>). An increased number of GFAP-IR and S100β-IR astrocytes in MSG2 and MSG4 groups is demonstrated. GFAP-IR astrocytes contain short and few processes. The arrows indicate the astrocytes. The asterisks indicate the neuronal fibers within the caudate nucleus. Scale bar 50 µm.</p> Full article ">Figure 2
<p>Average density of GFAP-IR astrocytes (<b>A</b>), average number of GFAP-IR astrocytic processes (<b>B</b>) and average density of S100β-IR astrocytes (<b>C</b>) in caudate nucleus of the studied groups of rats (Control, MSG2 and MSG4). Data show mean values with standard deviation. * Statistically significant differences between the studied groups, Kruskal–Wallis, <span class="html-italic">p</span> &lt; 0.05.</p> Full article ">Figure 3
<p>Optical density of GFAP-IR astrocytes (<b>A</b>) and S100β-IR astrocytes (<b>C</b>) in 100 cells divided between strong, moderate, weak and negative reaction intensity. An average optical density of GFAP-IR astrocytes (<b>B</b>) and average optical density of S100β-IR astrocytes (<b>D</b>) in the studied groups of rats (Control, MSG2, MSG4). Data in B and D show mean values with standard deviation. * Statistically significant differences between the studied groups, Kruskal–Wallis, <span class="html-italic">p</span> &lt; 0.05.</p> Full article ">
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