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Special Issue "A Special Class of Messenger Molecules in the Central Nervous System: The Neuropeptides at the Interplay between Function and Dysfunction"

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: 31 July 2019

Special Issue Editors

Guest Editor
Prof. Dr. Davide Cervia

Associate Professor of Physiology, Department for Innovation in Biological, Agro-food and Forest systems (DIBAF), University of Tuscia, Italy
Interests: neuroprotection, neurodegenerative and neuromuscular disorders, autophagy and apoptosis, signaling mechanisms of cell death/survival, natural compounds, tumor biology
Guest Editor
Prof. Dr. Giovanni Casini

Associate Professor of Physiology, Department of Biology, University of Pisa, Italy
Interests: neuroprotection, physiology and pathology of the retina, physiology and pathology of the neurovascular unit, regulation of growth factor expression, nutraceuticals

Special Issue Information

Dear Colleagues,

In the 1970s, an endogenous peptide was found in nerve cells, and the term “neuropeptide” was then introduced. Chemically, neuropeptides have a less complex three-dimensional structure and are smaller than normal proteins, but they are larger than classic neurotransmitters. More than 100 different neuropeptides are currently known to be involved in cell signaling. With some exceptions, almost all peptidergic receptors belong to the superfamily of G-protein-coupled receptors (GPCRs). Commonly, there are several receptor subtypes for a given peptide ligand, and many naturally occurring peptides exhibit a high degree of promiscuity across GPCRs.

After many years of intense research, there is a general agreement that neuropeptides are widely distributed throughout the central nervous system (CNS); they usually act as complementary signals to “classic” neurotransmitters to fine-tune neurotransmission, thereby controlling the balance between excitation and inhibition. In addition, there are well-documented reports of neuropeptides acting as neuroprotectants. Since neuropeptides and their receptors not only are present in neurons and glial cells but also are widely expressed in non-neural cells, neuropeptide functions range from neuromodulators to neuro-hormones, from immune-modulators to growth factors.

The aim of the present Special Issue is to explore and highlight the emerging roles of neuropeptide systems across several functions and dysfunctions of neurons and neural networks. The study of the impact of neuropeptides and their receptors on the pathogenesis of CNS disorders is an area that at present is almost totally unexplored, but, at the same time, may turn out to be extremely important in the design of new therapeutics. We invite authors to contribute with original research at the molecular, cellular, and tissue levels, that will help to better define the contribution of neuropeptides to various aspects of CNS physiopathology. The main goal is to highlight new insights in neuropeptide mechanisms that operate in the brain and that could be involved in human diseases. Reviews that summarize recent findings in both basic and clinical research and discuss current outcomes are also welcome.

Prof. Dr. Davide Cervia
Prof. Dr. Giovanni Casini
Guest Editors

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 papers will be 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. Journal of Clinical Medicine 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 1800 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.


  • Neuropeptides
  • GPCRs
  • CNS disorders
  • Brain function
  • Brain damage
  • Neuronal signaling
  • Neurotransmission and Neuromodulation
  • Neuroprotection

Published Papers (1 paper)

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Open AccessArticle
New Insights into the Mechanisms of Action of Topical Administration of GLP-1 in an Experimental Model of Diabetic Retinopathy
J. Clin. Med. 2019, 8(3), 339; https://doi.org/10.3390/jcm8030339
Received: 28 January 2019 / Revised: 4 March 2019 / Accepted: 7 March 2019 / Published: 11 March 2019
Cited by 1 | PDF Full-text (8631 KB) | HTML Full-text | XML Full-text
The main goals of this work were to assess whether the topical administration of glucagon-like peptide-1 (GLP-1) could revert the impairment of the neurovascular unit induced by long-term diabetes (24 weeks) in diabetic mice and to look into the underlying mechanisms. For that [...] Read more.
The main goals of this work were to assess whether the topical administration of glucagon-like peptide-1 (GLP-1) could revert the impairment of the neurovascular unit induced by long-term diabetes (24 weeks) in diabetic mice and to look into the underlying mechanisms. For that reason, db/db mice were treated with eye drops of GLP-1 or vehicle for 3 weeks. Moreover, db/+ mice were used as control. Studies performed in vivo included electroretinogramand the assessment of vascular leakage by using Evans Blue. NF-κB, GFAP and Ki67 proteins were analyzed by immunofluorescence (IF). Additionally, caspase 9, AMPK, IKBα, NF-κB, AKT, GSK3, β-catenin, Bcl-xl, and VEGF were analyzed by WB. Finally, VEGF, IL-1β, IL-6, TNF-α, IL-18, and NLRP3 were studied by reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence. We found that topical administration of GLP-1 reverted reactive gliosis and albumin extravasation, and protected against apoptosis and retinal dysfunction. Regarding the involved mechanisms, GLP-1 exerted an anti-inflammatory action by decreasing NF-κB, inflammosome, and pro-inflammatory factors. In addition, it also decreased VEGF expression. Furthermore, GLP-1 promoted cell survival by increasing the anti-apoptotic protein Bcl-xl and the signaling pathway Akt/GSK3b/β-catenin. Finally, Ki67 results revealed that GLP-1 treatment could induce neurogenesis. In conclusion, the topical administration of GLP-1 reverts the impairment of the neurovascular unit by modulating essential pathways involved in the development of diabetic retinopathy (DR). These beneficial effects on the neurovascular unit could pave the way for clinical trials addressed to confirm the effectiveness of GLP-1 in early stages of DR. Full article

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J. Clin. Med. EISSN 2077-0383 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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