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Biomedicines
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Neuropeptides in Health and Disease
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Neuropeptides in Health and Disease

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 8389

Special Issue Editor

Dr. Zsolt Bagosi

E-Mail Website
Guest Editor
Szegedi Tudományegyetem (SZTE), Szeged, Hungary
Interests: urocortins; stress; anxiety; depression; alcohol; nicotine

Special Issue Information

Dear Colleagues,

There are now over 100 discovered neuropeptides, and probably 1000 more are yet to be identified, predicted by the genes that encode them. Neuropeptides are synthesized by neurons and can be released locally in the brain, playing the role of a neurotransmitter, or peripherally into the circulation, acting as a neurohormone. Being expressed in many organs and tissues of the body, they can regulate physiological processes, such as stress responses, learning and memory, food and water intake, and social and sexual behavior. Nevertheless, they can also be involved in the pathomechanism of diseases, such as anxiety, depression, Alzheimer’s disease, diabetes mellitus and insipidus, autism and schizophrenia. In this Special Issue of Biomedicines, I would like to invite you to share your research regarding neuropeptides or neuropeptide families in the form of a review or original article revealing their physiological, pathophysiological and potential therapeutic roles in health and disease.

Dr. Zsolt Bagosi
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.

Published Papers (5 papers)

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Research

Jump to: Review

20 pages, 2461 KiB  
Article
A Brain Region-Dependent Alteration in the Expression of Vasopressin, Corticotropin-Releasing Factor, and Their Receptors Might Be in the Background of Kisspeptin-13-Induced Hypothalamic-Pituitary-Adrenal Axis Activation and Anxiety in Rats
by Krisztina Csabafi, Katalin Eszter Ibos, Éva Bodnár, Kata Filkor, Júlia Szakács and Zsolt Bagosi
Biomedicines 2023, 11(9), 2446; https://doi.org/10.3390/biomedicines11092446 - 02 Sep 2023
Viewed by 882
Abstract
Previously, we reported that intracerebroventricularly administered kisspeptin-13 (KP-13) induces anxiety-like behavior and activates the hypothalamic-pituitary-adrenal (HPA) axis in rats. In the present study, we aimed to shed light on the mediation of KP-13′s stress-evoking actions. The relative gene expressions of the corticotropin-releasing factor [...] Read more.
Previously, we reported that intracerebroventricularly administered kisspeptin-13 (KP-13) induces anxiety-like behavior and activates the hypothalamic-pituitary-adrenal (HPA) axis in rats. In the present study, we aimed to shed light on the mediation of KP-13′s stress-evoking actions. The relative gene expressions of the corticotropin-releasing factor (Crf, Crfr1, and Crfr2) and arginine vasopressin (Avp, Avpr1a, and Avpr1b) systems were measured in the amygdala and hippocampus of male Wistar rats after icv KP-13 treatment. CRF and AVP protein content were also determined. A different set of animals received CRF or V1 receptor antagonist pretreatment before the KP-13 challenge, after which either an open-field test or plasma corticosterone levels measurement was performed. In the amygdala, KP-13 induced an upregulation of Avp and Avpr1b expression, and a downregulation of Crf. In the hippocampus, the mRNA level of Crf increased and the level of Avpr1a decreased. A significant rise in AVP protein content was also detected in the amygdala. KP-13 also evoked anxiety-like behavior in the open field test, which the V1 receptor blocker antagonized. Both CRF and V1 receptor blockers reduced the KP-13-evoked rise in the plasma corticosterone level. This suggests that KP-13 alters the AVP and CRF signaling and that might be responsible for its effect on the HPA axis and anxiety-like behavior. Full article
(This article belongs to the Special Issue Neuropeptides in Health and Disease)
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12 pages, 7648 KiB  
Article
Inflammatory Orofacial Pain Activates Peptidergic Neurons and Upregulates the Oxytocin Receptor Expression in Trigeminal Ganglion
by Péter Bátor Kemenesi-Gedei, Krisztina Anna Csabafi and Gyöngyi Kis
Biomedicines 2023, 11(9), 2419; https://doi.org/10.3390/biomedicines11092419 - 29 Aug 2023
Cited by 1 | Viewed by 752
Abstract
The majority of orofacial pain is caused by musculoskeletal and neuropathological diseases related to inflammatory processes that lead even to transcriptional alterations in the trigeminal ganglion (TG) neurons. The hypothalamic nonapeptide oxytocin has been reported to modulate nociception via binding and activating its [...] Read more.
The majority of orofacial pain is caused by musculoskeletal and neuropathological diseases related to inflammatory processes that lead even to transcriptional alterations in the trigeminal ganglion (TG) neurons. The hypothalamic nonapeptide oxytocin has been reported to modulate nociception via binding and activating its receptor in primary sensory neurons. The purpose of this study was to analyze the gene expression of the oxytocin receptor (OTR), c-Fos, an indicator of neuronal activity, and α-calcitonin gene-related peptide (αCGRP), a characteristic neurotransmitter of the peptidergic trigeminal primary afferents in an animal model of inflammation-induced orofacial pain. Carrageenan was unilaterally injected into the vibrissal pads of male and female adult Wistar rats. RT-qPCR was performed to analyze the levels of mRNA expression in TGs 24 h after injection. The gene expression analysis revealed higher fold changes regarding the c-Fos (mean ± S.E: ♀: 3.9 ± 0.19; ♂: 3.55 ± 0.18) and αCGRP (♀: 2.84 ± 0.13; ♂: 3.39 ± 0.47) expression levels of mRNA, and a moderate rise in the expression of the OTR mRNA (♀: 1.52 ± 0.07; ♂: 1.49 ± 0.07) was observed in comparison to both vehicle(saline)-treated and untreated controls. Our results furnish evidence for inflammation-induced activation of peptidergic neurons, and it is suggested that oxytocin modulates inflammation-induced nociception by enhancing their signaling capacity due to its elevated expression in the sensory ganglion cells, thus providing new therapies for orofacial pain relief that target the OTRs. Full article
(This article belongs to the Special Issue Neuropeptides in Health and Disease)
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11 pages, 1570 KiB  
Article
Plasma Somatostatin Levels Increase during Scoliosis Surgery, but Not Herniated Disc Operations: Results of a Pilot Study
by Balázs Sütő, Bálint Kolumbán, Éva Szabó, Sára Pásztor, Timea Németh, Teréz Bagoly, Bálint Botz, Erika Pintér and Zsuzsanna Helyes
Biomedicines 2023, 11(8), 2154; https://doi.org/10.3390/biomedicines11082154 - 31 Jul 2023
Viewed by 903
Abstract
Somatostatin (SST) released from capsaicin-sensitive sensory nerves in response to stimulation exerts systemic anti-inflammatory, analgesic actions. Its elevation correlates with the extent of tissue injury. We measured plasma SST alterations during spine operations (scoliosis and herniated disc) to determine whether its release might [...] Read more.
Somatostatin (SST) released from capsaicin-sensitive sensory nerves in response to stimulation exerts systemic anti-inflammatory, analgesic actions. Its elevation correlates with the extent of tissue injury. We measured plasma SST alterations during spine operations (scoliosis and herniated disc) to determine whether its release might be a general protective mechanism during painful conditions. Sampling timepoints were baseline (1), after: soft tissue retraction (2), osteotomy (3), skin closure (4), the following morning (5). Plasma SST-like immunoreactivity (SST-LI) determined by radioimmunoassay was correlated with pain intensity and the correction angle (Cobb angle). In scoliosis surgery, postoperative pain intensity (VAS 2.) 1 day after surgery significantly increased (from 1.44 SEM ± 0.68 to 6.77 SEM ± 0.82, p = 0.0028) and positively correlated with the Cobb angle (p = 0.0235). The baseline Cobb degree negatively correlated (p = 0.0459) with the preoperative SST-LI. The plasma SST-LI significantly increased in fraction 3 compared to the baseline (p < 0.05), and significantly decreased thereafter (p < 0.001). In contrast, in herniated disc operations no SST-LI changes were observed in either group. The VAS decreased after surgery both in the traditional (mean 6.83 to 2.29, p = 0.0005) and microdiscectomy groups (mean 7.22 to 2.11, p = 0.0009). More extensive and destructive scoliosis surgery might cause greater tissue damage with greater pain (inflammation), which results in a significant SST release into the plasma from the sensory nerves. SST is suggested to be involved in an endogenous postoperative analgesic (anti-inflammatory) mechanism. Full article
(This article belongs to the Special Issue Neuropeptides in Health and Disease)
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Review

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37 pages, 2923 KiB  
Review
Vasopressin as Possible Treatment Option in Autism Spectrum Disorder
by Kristóf László, Dávid Vörös, Pedro Correia, Csilla Lea Fazekas, Bibiána Török, Imola Plangár and Dóra Zelena
Biomedicines 2023, 11(10), 2603; https://doi.org/10.3390/biomedicines11102603 - 22 Sep 2023
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Abstract
Autism spectrum disorder (ASD) is rather common, presenting with prevalent early problems in social communication and accompanied by repetitive behavior. As vasopressin was implicated not only in salt-water homeostasis and stress-axis regulation, but also in social behavior, its role in the development of [...] Read more.
Autism spectrum disorder (ASD) is rather common, presenting with prevalent early problems in social communication and accompanied by repetitive behavior. As vasopressin was implicated not only in salt-water homeostasis and stress-axis regulation, but also in social behavior, its role in the development of ASD might be suggested. In this review, we summarized a wide range of problems associated with ASD to which vasopressin might contribute, from social skills to communication, motor function problems, autonomous nervous system alterations as well as sleep disturbances, and altered sensory information processing. Beside functional connections between vasopressin and ASD, we draw attention to the anatomical background, highlighting several brain areas, including the paraventricular nucleus of the hypothalamus, medial preoptic area, lateral septum, bed nucleus of stria terminalis, amygdala, hippocampus, olfactory bulb and even the cerebellum, either producing vasopressin or containing vasopressinergic receptors (presumably V1a). Sex differences in the vasopressinergic system might underline the male prevalence of ASD. Moreover, vasopressin might contribute to the effectiveness of available off-label therapies as well as serve as a possible target for intervention. In this sense, vasopressin, but paradoxically also V1a receptor antagonist, were found to be effective in some clinical trials. We concluded that although vasopressin might be an effective candidate for ASD treatment, we might assume that only a subgroup (e.g., with stress-axis disturbances), a certain sex (most probably males) and a certain brain area (targeting by means of virus vectors) would benefit from this therapy. Full article
(This article belongs to the Special Issue Neuropeptides in Health and Disease)
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19 pages, 1394 KiB  
Review
The Role of Corticotropin-Releasing Factor (CRF) and CRF-Related Peptides in the Social Behavior of Rodents
by Zsolt Bagosi, Kíra Megyesi, Jázmin Ayman, Hanna Rudersdorf, Maieda Khan Ayaz and Krisztina Csabafi
Biomedicines 2023, 11(8), 2217; https://doi.org/10.3390/biomedicines11082217 - 07 Aug 2023
Viewed by 1216
Abstract
Since the corticotropin-releasing factor (CRF) was isolated from an ovine brain, a growing family of CRF-related peptides has been discovered. Today, the mammalian CRF system consists of four ligands (CRF, urocortin 1 (Ucn1), urocortin 2 (Ucn2), and urocortin 3 (Ucn3)); two receptors (CRF [...] Read more.
Since the corticotropin-releasing factor (CRF) was isolated from an ovine brain, a growing family of CRF-related peptides has been discovered. Today, the mammalian CRF system consists of four ligands (CRF, urocortin 1 (Ucn1), urocortin 2 (Ucn2), and urocortin 3 (Ucn3)); two receptors (CRF receptor type 1 (CRF1) and CRF receptor type 2 (CRF2)); and a CRF-binding protein (CRF-BP). Besides the regulation of the neuroendocrine, autonomic, and behavioral responses to stress, CRF and CRF-related peptides are also involved in different aspects of social behavior. In the present study, we review the experiments that investigated the role of CRF and the urocortins involved in the social behavior of rats, mice, and voles, with a special focus on sociability and preference for social novelty, as well as the ability for social recognition, discrimination, and memory. In general, these experiments demonstrate that CRF, Ucn1, Ucn2, and Ucn3 play important, but distinct roles in the social behavior of rodents, and that they are mediated by CRF1 and/or CRF2. In addition, we suggest the possible brain regions and pathways that express CRF and CRF-related peptides and that might be involved in social interactions. Furthermore, we also emphasize the differences between the species, strains, and sexes that make translation of these roles from rodents to humans difficult. Full article
(This article belongs to the Special Issue Neuropeptides in Health and Disease)
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