Neuropeptides and Psychiatric Disorders

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (1 October 2020) | Viewed by 3203

Special Issue Editor


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Guest Editor
INSB, UMR7275 Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Côte d’Azur, Valbonne 06560, France
Interests: pathologies associated with neuropeptides; pharmacology of depression; treatment-resistant depression; post-traumatic depression; markers for psychiatric diseases

Special Issue Information

Dear Colleagues,

The role of neuropeptides as neuromodulators in the brain is often complementary to classical neurotransmitters’ actions. In this context, neuropeptides have been shown to be involved in the pathophysiology of numerous psychiatric disorders, such as anxiety disorders, mood disorders (depression and bipolar disorder), personality disorders, eating disorders, psychotic disorders (schizophrenia), trauma-related disorders (post-traumatic stress or depression), substance abuse disorders, etc.

Due to the health burden of all these psychiatric pathologies, the further development of neuropeptide receptor agonists and/or antagonists with particular properties (such as the crossing of blood-brain barrier) appears crucial for the treatments and the diagnosis of the disorders. The present Special Issue aims to collect original research studies as well as review and perspective articles that provide future directions and advances for the use of neuropeptide ligands as therapeutic agents able to regulate the central and peripheral physiopathology of such disorders. Therefore, articles or reviews should not be restricted to central actions of neuropeptides but may also concern peripheral regulations that influence brain-related behaviors. We would like this Special Issue to become a major reference for those working in the field of neuropeptides associated pathologies.

Dr. Jean Mazella
Guest Editor

Manuscript Submission Information

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Keywords

  • Neuropeptide
  • Depression
  • Anxiety
  • Eating disorders
  • Post-traumatic depression
  • Schizophrenia
  • Agonist/antagonist
  • Blood–brain barrier

Published Papers (1 paper)

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Research

18 pages, 3977 KiB  
Article
DLK1 Expressed in Mouse Orexin Neurons Modulates Anxio-Depressive Behavior but Not Energy Balance
by Tatiyana Harris, Raluca Bugescu, Jaylyn Kelly, Anna Makela, Morgan Sotzen, Cheryl Sisk, Graham Atkin, Rebecca Pratt, Elahé Crockett and Gina Leinninger
Brain Sci. 2020, 10(12), 975; https://doi.org/10.3390/brainsci10120975 - 12 Dec 2020
Cited by 3 | Viewed by 2849
Abstract
Lateral hypothalamic area (LHA) neurons expressing the neuropeptide orexin (OX) are implicated in obesity and anxio-depression. However, these neurons release OX as well as a host of other proteins that might contribute to normal physiology and disease states. We hypothesized that delta-like homolog [...] Read more.
Lateral hypothalamic area (LHA) neurons expressing the neuropeptide orexin (OX) are implicated in obesity and anxio-depression. However, these neurons release OX as well as a host of other proteins that might contribute to normal physiology and disease states. We hypothesized that delta-like homolog 1 (DLK1), a protein reported to be co-expressed by all OX neurons, contributes to the regulation of energy balance and/or anxio-depression. Consistent with previous reports, we found that all rat OX neurons co-express DLK1. Yet, in mice and humans only a subset of OX neurons co-expressed DLK1. Since human OX-DLK1 distribution is more similar to mice than rats, mice are a comparable model to assess the human physiologic role of DLK1. We therefore used a viral lesion strategy to selectively delete DLK1 within the LHA of adult mice (DLK1Null) to reveal its role in body weight and behavior. Adult-onset DLK1 deletion had no impact on body weight or ingestive behavior. However, DLK1Null mice engaged in more locomotor activity than control mice and had decreased anxiety and depression measured via the elevated plus maze and forced swim tests. These data suggest that DLK1 expression via DLK1-expressing OX neurons primarily contributes to anxio-depression behaviors without impacting body weight. Full article
(This article belongs to the Special Issue Neuropeptides and Psychiatric Disorders)
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