ijms-logo

Journal Browser

Journal Browser

Kinase-Mediated Signaling in Mood Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (15 January 2023) | Viewed by 2823

Special Issue Editors


E-Mail Website
Guest Editor
Department of Experimental and Clinical Medicine, University of Pisa, Pisa, Italy
Interests: behavioral epigenetics

E-Mail Website
Guest Editor
Department of Surgical, Medical and Molecular Pathology and Critical Care Medicine, University of Pisa, 56124 Pisa, Italy
Interests: neurobiology of psychopathology; human social behavior
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Disruptions of brain cell metabolism, microstructure, and neurotransmission underly the onset of psychiatric disorders. These processes underly various kinase-mediated signaling events. Altered serine–threonine kinase activity plays an important role in several mood disorders, and psychotropic drugs such as lithium and valproic acid decrease protein kinase (PK) signaling. In particular, the selective inhibition of PKC seems to be implicated in the resolution of manic symptoms.

Kinases are a family of proteins catalyzing the phosphorylation reaction on tyrosine and serine/threonine protein residues and functioning as mediators of multiple molecular pathways involved in the regulation of several biological processes disrupted in mood disorders, including cellular homeostasis, molecular trafficking, inter-cellular signaling, synaptogenesis, synaptic functioning, neurogenesis, and neuronal migration, all of which are essential for optimal brain development and neurotransmission.

The factors implicated in the activation of PKC as well as the downstream targets of PKC remain to be clearly identified; additional research is warranted and may lead to the identification of novel therapeutic targets.

Basic research studies in vitro, ex vivo, or in vivo, in animals or humans, as well as reviews discussing the role of PKC in biological processes, pharmacological treatment, behavior, and psychiatry are welcome.

Bullet point topics:

  • PKC-mediated phosphorylation of GSK-3β;
  • Serine and Tyrosine phosphorylation of GSK-3β;
  • AKT and mTOR expression and phosphorylation;
  • Activation of PI3K and AKTs;
  • Role of PKC in mood disorders (schizophrenia, bipolar disorder and mania);
  • Pharmacological treatments targeting PKC/

Dr. Silvia Pellegrini 
Dr. Sara Palumbo
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 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

  • kinases
  • PKC
  • mood disorders
  • GSK-3β
  • schizophrenia
  • bipolar disorder and mania
  • AKT
  • mTOR

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Other

12 pages, 766 KiB  
Perspective
Esmethadone (REL-1017) and Other Uncompetitive NMDAR Channel Blockers May Improve Mood Disorders via Modulation of Synaptic Kinase-Mediated Signaling
by Stephen M. Stahl, Sara De Martin, Andrea Mattarei, Ezio Bettini, Luca Pani, Clotilde Guidetti, Franco Folli, Marc de Somer, Sergio Traversa, Charles E. Inturrisi, Marco Pappagallo, Marco Gentilucci, Andrea Alimonti, Maurizio Fava and Paolo L. Manfredi
Int. J. Mol. Sci. 2022, 23(20), 12196; https://doi.org/10.3390/ijms232012196 - 13 Oct 2022
Cited by 8 | Viewed by 2518
Abstract
This article presents a mechanism of action hypothesis to explain the rapid antidepressant effects of esmethadone (REL-1017) and other uncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonists and presents a corresponding mechanism of disease hypothesis for major depressive disorder (MDD). Esmethadone and other uncompetitive NMDAR antagonists [...] Read more.
This article presents a mechanism of action hypothesis to explain the rapid antidepressant effects of esmethadone (REL-1017) and other uncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonists and presents a corresponding mechanism of disease hypothesis for major depressive disorder (MDD). Esmethadone and other uncompetitive NMDAR antagonists may restore physiological neural plasticity in animal models of depressive-like behavior and in patients with MDD via preferential tonic block of pathologically hyperactive GluN2D subtypes. Tonic Ca2+ currents via GluN2D subtypes regulate the homeostatic availability of synaptic proteins. MDD and depressive behaviors may be determined by reduced homeostatic availability of synaptic proteins, due to upregulated tonic Ca2+ currents through GluN2D subtypes. The preferential activity of low-potency NMDAR antagonists for GluN2D subtypes may explain their rapid antidepressant effects in the absence of dissociative side effects. Full article
(This article belongs to the Special Issue Kinase-Mediated Signaling in Mood Disorders)
Show Figures

Figure 1

Back to TopTop