Drug Effects on Neuroendocrine Regulation: New Development

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1403

Special Issue Editors

Department of Pharmacy, “G. d'Annunzio” University, Via dei Vestini 31, 66100 Chieti, Italy
Interests: neuroendocrine regulation; GHRH deficiency; feeding
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Guest Editor
Department of Pharmacy, “G. d’Annunzio” University, Via dei Vestini 31, 66100 Chieti, Italy
Interests: neuroendocrine regulation; GHRH deficiency; feeding
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute original research papers or review articles to the Special Issue “Drug Effects on Neuroendocrine Regulation”.

It is well known that whole-body homeostasis is finely modulated by the interplay of nervous and endocrine systems.  In this context, studies have shown that neuroendocrine dysregulation could affect onset and progression of various diseases, such as cancer, neurological and psychiatric disorders, polycystic ovary syndrome, metabolic and cardiovascular diseases.

The aim of this Special Issue is to further deepen current knowledge and new strategies for the prevention and treatment of neuroendocrine-related disorders.

Prof. Dr. Luigi Brunetti
Dr. Sheila Leone
Dr. Lucia Recinella
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • neuroendocrine regulation
  • hormones
  • neuropeptides
  • neurotransmitters
  • molecular pathways
  • drugs

Published Papers (1 paper)

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Research

13 pages, 2159 KiB  
Article
Effects of GHRH Deficiency and GHRH Antagonism on Emotional Disorders in Mice
by Lucia Recinella, Maria Loreta Libero, Serena Veschi, Anna Piro, Guya Diletta Marconi, Francesca Diomede, Annalisa Chiavaroli, Giustino Orlando, Claudio Ferrante, Rosalba Florio, Alessia Lamolinara, Renzhi Cai, Wei Sha, Andrew V. Schally, Roberto Salvatori, Luigi Brunetti and Sheila Leone
Cells 2023, 12(22), 2615; https://doi.org/10.3390/cells12222615 - 12 Nov 2023
Viewed by 1106
Abstract
Growth hormone (GH)-releasing hormone (GHRH) has been suggested to play a crucial role in brain function. We aimed to further investigate the effects of a novel GHRH antagonist of the Miami (MIA) series, MIA-602, on emotional disorders and explore the relationships between the [...] Read more.
Growth hormone (GH)-releasing hormone (GHRH) has been suggested to play a crucial role in brain function. We aimed to further investigate the effects of a novel GHRH antagonist of the Miami (MIA) series, MIA-602, on emotional disorders and explore the relationships between the endocrine system and mood disorders. In this context, the effects induced by MIA-602 were also analyzed in comparison to vehicle-treated mice with GH deficiency due to generalized ablation of the GHRH gene (GHRH knock out (GHRHKO)). We show that the chronic subcutaneous administration of MIA-602 to wild type (+/+) mice, as well as generalized ablation of the GHRH gene, is associated with anxiolytic and antidepressant behavior. Moreover, immunohistochemical and Western blot analyses suggested an evident activation of Nrf2, HO1, and NQO1 in the prefrontal cortex of both +/+ mice treated with MIA-602 (+/+ MIA-602) and homozygous GHRHKO (−/− control) animals. Finally, we also found significantly decreased COX-2, iNOS, NFkB, and TNF-α gene expressions, as well as increased P-AKT and AKT levels in +/+ MIA-602 and −/− control animals compared to +/+ mice treated with vehicle (+/+ control). We hypothesize that the generalized ablation of the GHRH gene leads to a dysregulation of neural pathways, which is mimicked by GHRH antagonist treatment. Full article
(This article belongs to the Special Issue Drug Effects on Neuroendocrine Regulation: New Development)
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