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Serotonin Receptors in Human Health and Disease
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Serotonin Receptors in Human Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 December 2023) | Viewed by 7426

Special Issue Editor

Prof. Dr. Natalija Filipović

E-Mail Website
Guest Editor
Department of Anatomy, Histology and Embryology, University of Split School of Medicine, Šoltanska 2, 21000 Split, Croatia
Interests: microvascular and macrovascular complications of diabetes; diabetic nephropathy; renal physiology and pathology; gene expression during embryonic and foetal development; kidneys and urinary system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Serotonin (5-hydroxytryptamine (5- HT)) is a monoamine that acts as a neurotransmitter at neuronal synapses, but it also plays an important role in a variety of different organ systems. Its action is involved in the regulation of many physiological processes, including appetite, sleep, mood, nociception, stress response, blood pressure and vasomotility, heart rate and pulmonary function, gastrointestinal motility, micturition, and reproductive function. In addition, serotonin has also been found to play an important role in the development of the nervous system and various other organs. Serotonin acts through a group of receptors that are widely distributed in various organs. All serotonin receptors are G-protein-coupled receptors, with the exception of the 5-HT3 receptor, which is a ligand-gated ion channel. To date, 14 different subtypes have been identified, divided into 7 families (5-HT1-7), with different pharmacological effects. The signaling mechanism of serotonin receptors has also been found to depend on their conformational plasticity. Despite the extensive research, our knowledge of the amazing diversity of functions of serotonin and its receptors is far from complete, and much research is still needed to fill this gap. Therefore, we cordially invite researchers to submit review articles or original papers that contribute to our knowledge and understanding of the structure, function, and role of serotonin receptors in various pathologies. Potential topics include, but are not limited to, the following: functions in the nervous system; cardiovascular regulation; gastrointestinal and other visceral functions; mechanisms of action; role in development; future perspectives for pharmacotherapy.

Prof. Dr. Natalija Filipović
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

  • serotonin
  • serotonin receptors
  • brain
  • pharmacology

Published Papers (4 papers)

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Research

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20 pages, 6662 KiB  
Article
Limbic System Response to Psilocybin and Ketamine Administration in Rats: A Neurochemical and Behavioral Study
by Adam Wojtas, Agnieszka Bysiek, Agnieszka Wawrzczak-Bargiela, Marzena Maćkowiak and Krystyna Gołembiowska
Int. J. Mol. Sci. 2024, 25(1), 100; https://doi.org/10.3390/ijms25010100 (registering DOI) - 20 Dec 2023
Cited by 1 | Viewed by 1270
Abstract
The pathophysiology of depression is related to the reduced volume of the hippocampus and amygdala and hypertrophy of the nucleus accumbens. The mechanism of these changes is not well understood; however, clinical studies have shown that the administration of the fast-acting antidepressant ketamine [...] Read more.
The pathophysiology of depression is related to the reduced volume of the hippocampus and amygdala and hypertrophy of the nucleus accumbens. The mechanism of these changes is not well understood; however, clinical studies have shown that the administration of the fast-acting antidepressant ketamine reversed the decrease in hippocampus and amygdala volume in depressed patients, and the magnitude of this effect correlated with the reduction in depressive symptoms. In the present study, we attempted to find out whether the psychedelic substance psilocybin affects neurotransmission in the limbic system in comparison to ketamine. Psilocybin and ketamine increased the release of dopamine (DA) and serotonin (5-HT) in the nucleus accumbens of naive rats as demonstrated using microdialysis. Both drugs influenced glutamate and GABA release in the nucleus accumbens, hippocampus and amygdala and increased ACh levels in the hippocampus. The changes in D2, 5-HT1A and 5-HT2A receptor density in the nucleus accumbens and hippocampus were observed as a long-lasting effect. A marked anxiolytic effect of psilocybin in the acute phase and 24 h post-treatment was shown in the open field test. These data provide the neurobiological background for psilocybin’s effect on stress, anxiety and structural changes in the limbic system and translate into the antidepressant effect of psilocybin in depressed patients. Full article
(This article belongs to the Special Issue Serotonin Receptors in Human Health and Disease)
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16 pages, 2524 KiB  
Article
Transcriptional Regulation of the Human 5-HT1A Receptor Gene by Lithium: Role of Deaf1 and GSK3β
by Emerson F. Harkin, Georges Nasrallah, Brice Le François and Paul R. Albert
Int. J. Mol. Sci. 2023, 24(21), 15620; https://doi.org/10.3390/ijms242115620 - 26 Oct 2023
Viewed by 991
Abstract
Serotonin 1A (5-HT1A) autoreceptors located on serotonin neurons inhibit their activity, and their upregulation has been implicated in depression, suicide and resistance to antidepressant treatment. Conversely, post-synaptic 5-HT1A heteroreceptors are important for antidepressant response. The transcription factor deformed epidermal autoregulatory factor 1 (Deaf1) [...] Read more.
Serotonin 1A (5-HT1A) autoreceptors located on serotonin neurons inhibit their activity, and their upregulation has been implicated in depression, suicide and resistance to antidepressant treatment. Conversely, post-synaptic 5-HT1A heteroreceptors are important for antidepressant response. The transcription factor deformed epidermal autoregulatory factor 1 (Deaf1) acts as a presynaptic repressor and postsynaptic enhancer of 5-HT1A transcription, but the mechanism is unclear. Because Deaf1 interacts with and is phosphorylated by glycogen synthase kinase 3β (GSK3β)—a constitutively active protein kinase that is inhibited by the mood stabilizer lithium at therapeutic concentrations—we investigated the role of GSK3β in Deaf1 regulation of human 5-HT1A transcription. In 5-HT1A promoter-reporter assays, human HEK293 kidney and 5-HT1A-expressing SKN-SH neuroblastoma cells, transfection of Deaf1 reduced 5-HT1A promoter activity by ~45%. To identify potential GSK3β site(s) on Deaf1, point mutations of known and predicted phosphorylation sites on Deaf1 were tested. Deaf1 repressor function was not affected by any of the mutants tested except the Y300F mutant, which augmented Deaf1 repression. Both lithium and the selective GSK3 inhibitors CHIR-99021 and AR-014418 attenuated and reversed Deaf1 repression compared to vector. This inhibition was at concentrations that maximally inhibit GSK3β activity as detected by the GSK3β-sensitive TCF/LEF reporter construct. Our results support the hypothesis that GSK3β regulates the activity of Deaf1 to repress 5-HT1A transcription and provide a potential mechanism for actions of GSK3 inhibitors on behavior. Full article
(This article belongs to the Special Issue Serotonin Receptors in Human Health and Disease)
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20 pages, 15223 KiB  
Article
Expression Patterns of Serotonin Receptors 5-HT1A, 5-HT2A, and 5-HT3A during Human Fetal Lung Development
by Jelena Nikolić, Katarina Vukojević, Violeta Šoljić, Josip Mišković, Martina Orlović Vlaho, Mirna Saraga-Babić and Natalija Filipović
Int. J. Mol. Sci. 2023, 24(3), 2965; https://doi.org/10.3390/ijms24032965 - 03 Feb 2023
Cited by 2 | Viewed by 1814
Abstract
We analyzed the expression of the serotonin receptors 5-HT1A, 5-HT2A, and 5-HT3A at four different stages of fetal lung development from 12 to 40 weeks of gestation, divided into four groups: the pseudoglandular stage (12–16th week of development; n = 8), the canalicular [...] Read more.
We analyzed the expression of the serotonin receptors 5-HT1A, 5-HT2A, and 5-HT3A at four different stages of fetal lung development from 12 to 40 weeks of gestation, divided into four groups: the pseudoglandular stage (12–16th week of development; n = 8), the canalicular stage (16th–26th week of development; n = 7), the saccular stage (26th-36th week of development; n = 5), and the alveolar stage (36th–40th week of development; n = 5). The strongest expression of all three receptor types was found in the epithelium of the proximal airways during the pseudoglandular, canalicular, and saccular stages and in a vascular wall. 5-HT1A was also strongly expressed in the smooth muscle cells of the proximal airway. Vascular smooth muscle cells and endothelium occasionally showed a strong expression of 5-HT1A and 5-HT2A. In the alveolar stage, the expression of 5-HT1A, 5-HT2A, and 5-HT3A was detected in both type I (p1) and type II (p2) pneumocytes, with a stronger expression in p2. A significant decrease in percent the 5-HT2A area and in the integrated density was observed at the alveolar stage. On the other hand, a significant decrease in the percentage area but an increase in the integrated density was observed for 5-HT3A toward the alveolar stage, suggesting that a smaller number of cells expressed 5-HT3A but that they (p1 and p2) significantly increased their 5-HT3A expression at the alveolar stage. The results presented provided us with new data on the development and function of the serotonin system in the human fetal lung and gave us insight into their possible involvement in the pathogenesis of lung pathology, particularly that characteristic of the neonatal period. Full article
(This article belongs to the Special Issue Serotonin Receptors in Human Health and Disease)
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Review

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21 pages, 710 KiB  
Review
Therapeutic Potential and Limitation of Serotonin Type 7 Receptor Modulation
by Kouji Fukuyama, Eishi Motomura and Motohiro Okada
Int. J. Mol. Sci. 2023, 24(3), 2070; https://doi.org/10.3390/ijms24032070 - 20 Jan 2023
Cited by 6 | Viewed by 2470
Abstract
Although a number of mood-stabilising atypical antipsychotics and antidepressants modulate serotonin type 7 receptor (5-HT7), the detailed contributions of 5-HT7 function to clinical efficacy and pathophysiology have not been fully understood. The mood-stabilising antipsychotic agent, lurasidone, and the serotonin partial agonist reuptake inhibitor, [...] Read more.
Although a number of mood-stabilising atypical antipsychotics and antidepressants modulate serotonin type 7 receptor (5-HT7), the detailed contributions of 5-HT7 function to clinical efficacy and pathophysiology have not been fully understood. The mood-stabilising antipsychotic agent, lurasidone, and the serotonin partial agonist reuptake inhibitor, vortioxetine, exhibit higher binding affinity to 5-HT7 than other conventional antipsychotics and antidepressants. To date, the initially expected rapid onset of antidepressant effects—in comparison with conventional antidepressants or mood-stabilising antipsychotics—due to 5-HT7 inhibition has not been observed with lurasidone and vortioxetine; however, several clinical studies suggest that 5-HT7 inhibition likely contributes to quality of life of patients with schizophrenia and mood disorders via the improvement of cognition. Furthermore, recent preclinical studies reported that 5-HT7 inhibition might mitigate antipsychotic-induced weight gain and metabolic complication by blocking other monoamine receptors. Further preclinical studies for the development of 5-HT7 modulation against neurodevelopmental disorders and neurodegenerative diseases have been ongoing. To date, various findings from various preclinical studies indicate the possibility that 5-HT7 modifications can provide two independent strategies. The first is that 5-HT7 inhibition ameliorates the dysfunction of inter-neuronal transmission in mature networks. The other is that activation of 5-HT7 can improve transmission dysfunction due to microstructure abnormality in the neurotransmission network—which could be unaffected by conventional therapeutic agents—via modulating intracellular signalling during the neurodevelopmental stage or via loss of neural networks with aging. This review attempts to describe the current and novel clinical applications of 5-HT7 modulation based on preclinical findings. Full article
(This article belongs to the Special Issue Serotonin Receptors in Human Health and Disease)
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