For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
0
views
20
references
 Top references
cited by
0
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      171
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The dopamine 3 receptor as a candidate biomarker and therapeutic for opioid use disorder

      research-article
      Author(s): 1 , 2 ,
      Publication date (Electronic):
      Journal: Addiction Biology
      Publisher: John Wiley and Sons Inc.
      Keywords: genetic risk, opioid, opioid use disorder, pharmacogenetics

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Here, we present recent studies suggesting that specific DRD3 single nucleotide polymorphisms (SNPs, e.g. rs324029 and rs2654754) might serve as prognostic biomarkers for opioid use disorder (OUD). Additionally, preclinical studies with novel dopamine 3 receptor (D3R) partial agonists and antagonists have been evaluated as candidate OUD therapeutics and have shown a reduced risk of cardiovascular toxicity compared with the original D3R antagonist. From these findings, we argue that DRD3 SNPs could serve as a diagnostic tool for assessing OUD risk and that more research is warranted examining the D3R as a safe and effective therapeutic target for treating OUD.

          Abstract

          Recent studies suggest that specific DRD3 single nucleotide polymorphisms (SNPs) might serve as prognostic biomarkers for opioid use disorder (OUD). Preclinical studies with novel D3R partial agonists and antagonists have been evaluated as candidate OUD therapeutics. From these findings, we argue that DRD3 SNPs could serve as a diagnostic tool for assessing OUD risk and that more research is warranted examining the D3R as a safe and effective therapeutic target for treating OUD.

          Related collections

          Most cited references20

          • Record: found
          • Abstract: not found
          • Article: not found

          Comparative Effectiveness of Different Treatment Pathways for Opioid Use Disorder

          Sarah E Wakeman, Marc R Larochelle, Omid Ameli … (2020)
          Article 0 comments Cited 239 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Opioids excite dopamine neurons by hyperpolarization of local interneurons.

            SW Johnson, RA North (1992)
            Increased activity of dopamine-containing neurons in the ventral tegmental area is necessary for the reinforcing effects of opioids and other abused drugs. Intracellular recordings from these cells in slices of rat brain in vitro showed that opioids do not affect the principal (dopamine-containing) neurons but hyperpolarize secondary (GABA-containing) interneurons. Experiments with agonists and antagonists selective for opioid receptor subtypes indicated that the hyperpolarization of secondary cells involved the mu-receptor. Most principal cells showed spontaneous bicuculline-sensitive synaptic potentials when the extracellular potassium concentration was increased from 2.5 to 6.5 or 10.5 mM; these were prevented by TTX and assumed to result from action potentials arising in slightly depolarized local interneurons. The frequency of these synaptic potentials, but not their amplitudes, was reduced by opioids selective for mu-receptors. It is concluded that hyperpolarization of the interneurons by opioids reduces the spontaneous GABA-mediated synaptic input to the dopamine cells. In vivo, this would lead to excitation of the dopamine cells by disinhibition, which would be expected to contribute to the positive reinforcement seen with mu-receptor agonists such as morphine and heroin.
            Article 0 comments Cited 226 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The dopamine theory of addiction: 40 years of highs and lows.

              David J Nutt, Anne Lingford-Hughes, David Erritzoe … (2015)
              For several decades, addiction has come to be viewed as a disorder of the dopamine neurotransmitter system; however, this view has not led to new treatments. In this Opinion article, we review the origins of the dopamine theory of addiction and discuss the ability of addictive drugs to elicit the release of dopamine in the human striatum. There is robust evidence that stimulants increase striatal dopamine levels and some evidence that alcohol may have such an effect, but little evidence, if any, that cannabis and opiates increase dopamine levels. Moreover, there is good evidence that striatal dopamine receptor availability and dopamine release are diminished in individuals with stimulant or alcohol dependence but not in individuals with opiate, nicotine or cannabis dependence. These observations have implications for understanding reward and treatment responses in various addictions.
              Article 0 comments Cited 166 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Jon E. Sprague:
                ORCID: https://orcid.org/0000-0003-0349-5072
                jesprag@bgsu.edu
                Journal
                Journal ID (nlm-ta): Addict Biol
                Journal ID (iso-abbrev): Addict Biol
                Journal ID (doi): 10.1111/(ISSN)1369-1600
                Journal ID (publisher-id): ADB
                Title: Addiction Biology
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1355-6215
                ISSN (Electronic): 1369-1600
                Publication date (Electronic): 28 January 2024
                Publication date Collection: February 2024
                Volume: 29
                Issue: 2 ( doiID: 10.1111/adb.v29.2 )
                Electronic Location Identifier: e13369
                Affiliations
                [ 1 ] Department of Pharmacology and Toxicology Virginia Commonwealth University Richmond Virginia USA
                [ 2 ] The Ohio Attorney General's Center for the Future of Forensic Science Bowling Green State University Bowling Green Ohio USA
                Author notes
                [*] [* ] Correspondence

                Jon E. Sprague, The Ohio Attorney General's Center for the Future of Forensic Science, Bowling Green State University, Bowling Green, OH 43403, USA.

                Email: jesprag@ 123456bgsu.edu

                Author information
                https://orcid.org/0000-0003-0349-5072
                Article
                Publisher ID: ADB13369
                DOI: 10.1111/adb.13369
                PMC ID: 10883601
                PubMed ID: 38380709
                SO-VID: 2b2de922-7900-40dc-90cc-e5c87fe01b76
                Copyright © © 2024 The Authors. Addiction Biology published by John Wiley & Sons Ltd on behalf of Society for the Study of Addiction.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                Date revision received : 09 November 2023
                Date received : 19 July 2023
                Date accepted : 13 December 2023
                Page count
                Figures: 2, Tables: 1, Pages: 4, Words: 2889
                Funding
                Funded by: National Institutes of Health , doi 10.13039/100000002;
                Funded by: Ohio Attorney General , doi 10.13039/100024619;
                Funded by: National Institute on Drug Abuse , doi 10.13039/100000026;
                Award ID: P30DA033934
                Award ID: UH3DA050311
                Categories
                Subject: Perspective
                Subject: Perspective
                Custom metadata
                source-schema-version-number 2.0
                cover-date February 2024
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.3.8 mode:remove_FC converted:14.02.2024

                ScienceOpen disciplines: Health & Social care
                Keywords: genetic risk,opioid,opioid use disorder,pharmacogenetics
                Data availability:
                ScienceOpen disciplines: Health & Social care
                Keywords: genetic risk, opioid, opioid use disorder, pharmacogenetics

                Comments

                Comment on this article