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      Role of GPR39 in Neurovascular Homeostasis and Disease

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          Abstract

          GPR39, a member of the ghrelin family of G protein-coupled receptors, is zinc-responsive and contributes to the regulation of diverse neurovascular and neurologic functions. Accumulating evidence suggests a role as a homeostatic regulator of neuronal excitability, vascular tone, and the immune response. We review GPR39 structure, function, and signaling, including constitutive activity and biased signaling, and summarize its expression pattern in the central nervous system. We further discuss its recognized role in neurovascular, neurological, and neuropsychiatric disorders.

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          A neurotrophic model for stress-related mood disorders.

          Ronald S. Duman, Lisa M. Monteggia (2006)
          There is a growing body of evidence demonstrating that stress decreases the expression of brain-derived neurotrophic factor (BDNF) in limbic structures that control mood and that antidepressant treatment reverses or blocks the effects of stress. Decreased levels of BDNF, as well as other neurotrophic factors, could contribute to the atrophy of certain limbic structures, including the hippocampus and prefrontal cortex that has been observed in depressed subjects. Conversely, the neurotrophic actions of antidepressants could reverse neuronal atrophy and cell loss and thereby contribute to the therapeutic actions of these treatments. This review provides a critical examination of the neurotrophic hypothesis of depression that has evolved from this work, including analysis of preclinical cellular (adult neurogenesis) and behavioral models of depression and antidepressant actions, as well as clinical neuroimaging and postmortem studies. Although there are some limitations, the results of these studies are consistent with the hypothesis that decreased expression of BDNF and possibly other growth factors contributes to depression and that upregulation of BDNF plays a role in the actions of antidepressant treatment.
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            Trends in GPCR drug discovery: new agents, targets and indications

            Alexander S Hauser, Misty Attwood, Mathias Rask-Andersen … (2017)
            G protein-coupled receptors (GPCRs) are the most intensively studied drug targets, largely due to their substantial involvement in human pathophysiology and their pharmacological tractability. Here, we report the first analysis of all GPCR drugs and agents in clinical trials. This reveals the current trends across molecule types, drug targets and therapeutic indications, including showing that 481 drugs (~34% of all drugs approved by the FDA) act at 107 unique GPCR targets. Approximately 320 agents are currently in clinical trials, of which ~36% target 64 potentially novel GPCR targets without an approved drug, and the number of biological drugs, allosteric modulators and biased agonists has grown. The major disease indications for GPCR modulators show a shift towards diabetes, obesity, and Alzheimer’s disease, while other central nervous system disorders remain highly represented. The 227 (57%) non-olfactory GPCRs that are yet to be explored in clinical trials have broad untapped therapeutic potential, particularly in genetic and immune system disorders. Finally, we provide an interactive online resource to analyse and infer trends in GPCR drug discovery.
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              Function and regulation of CREB family transcription factors in the nervous system.

              Bonnie Lonze, David D. Ginty (2002)
              CREB and its close relatives are now widely accepted as prototypical stimulus-inducible transcription factors. In many cell types, these factors function as effector molecules that bring about cellular changes in response to discrete sets of instructions. In neurons, a wide range of extracellular stimuli are capable of activating CREB family members, and CREB-dependent gene expression has been implicated in complex and diverse processes ranging from development to plasticity to disease. In this review, we focus on the current level of understanding of where, when, and how CREB family members function in the nervous system.
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                Author and article information

                Contributors
                Anuska V. Andjelkovic: Role: Academic Editor
                Richard F. Keep: Role: Academic Editor
                Michael M. Wang: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 30 July 2021
                Publication date Collection: August 2021
                Volume: 22
                Issue: 15
                Electronic Location Identifier: 8200
                Affiliations
                [1 ]Department of Anesthesiology and Perioperative Medicine, Oregon Health and Science University, Portland, OR 97239, USA; xyi@ 123456ohsu.edu
                [2 ]Knight Cardiovascular Institute, Oregon Health and Science University, Portland, OR 97239, USA; barnesan@ 123456ohsu.edu
                Author notes
                [* ]Correspondence: alkayedn@ 123456ohsu.edu
                Author information
                https://orcid.org/0000-0002-3136-8858
                https://orcid.org/0000-0002-3489-4730
                Article
                Publisher ID: ijms-22-08200
                DOI: 10.3390/ijms22158200
                PMC ID: 8346997
                PubMed ID: 34360964
                SO-VID: 4809a7b5-4f67-4faa-93a2-ed34ac58f093
                Copyright © © 2021 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 07 July 2021
                Date accepted : 26 July 2021
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: gpr39,zinc,eicosanoids,biased agonist,dementia,vascular tone,depression,epilepsy
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: gpr39, zinc, eicosanoids, biased agonist, dementia, vascular tone, depression, epilepsy

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