Novel function of the poly(C)‐binding protein αCP3 as a transcriptional repressor of the mu opioid receptor gene

2007 ◽  
Vol 21 (14) ◽  
pp. 3963-3973 ◽  
Author(s):  
Hack Sun Choi ◽  
Chun Sung Kim ◽  
Cheol Kyu Hwang ◽  
Kyu Young Song ◽  
Ping‐Yee Law ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Binding Protein ◽  
Receptor Gene ◽  
Transcriptional Repressor ◽  
Mu Opioid Receptor ◽  
Mu Opioid

scholarly journals Variation of the human mu-opioid receptor (OPRM1) gene predicts vulnerability to frustration

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Alan M. Daniel ◽  
Brenda G. Rushing ◽  
Karla Y. Tapia Menchaca
Keyword(s):  
Individual Differences ◽  
Animal Models ◽  
Opioid Receptor ◽  
Receptor Gene ◽  
Emotional Reaction ◽  
Mu Opioid Receptor ◽  
Reward Processing ◽  
Physical Pain ◽  
Mu Opioid ◽  
Allelic Differences

AbstractUnderstanding the emotional reaction to loss, or frustration, is a critical problem for the field of mental health. Animal models of loss have pointed to the opioid system as a nexus of frustration, physical pain, and substance abuse. However, few attempts have been made to connect the results of animal models of loss to human behavior. Allelic differences in the human mu opioid receptor gene, notably the A118G single nucleotide polymorphism, have been linked to individual differences in pain sensitivity, depressive symptoms, and reward processing. The present study explored the relationship between A118G and behavior in two frustrating tasks in humans. Results showed that carriers of the mutant G-allele were slower to recover behavior following a reward downshift and abandoned a frustrating task earlier than those without the mutation. Additionally, G-carriers were more sensitive to physical pain. These results highlight the overlap between frustration and pain, and suggest that genetic variation in opioid tone may contribute to individual differences in vulnerability and resilience following emotional disturbances.

A118G Single Nucleotide Polymorphism of Human μ-Opioid Receptor Gene Influences Pain Perception and Patient-controlled Intravenous Morphine Consumption after Intrathecal Morphine for Postcesarean Analgesia

2008 ◽  
Vol 109 (3) ◽  
pp. 520-526 ◽  
Author(s):  
Alex T. Sia ◽  
Yvonne Lim ◽  
Eileen C. P. Lim ◽  
Rachelle W. C. Goh ◽  
Hai Yang Law ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Pain Perception ◽  
Intrathecal Morphine ◽  
Receptor Gene ◽  
Mu Opioid Receptor ◽  
Morphine Consumption ◽  
Mu Opioid ◽  
Pain Scores ◽  
Significant Difference ◽  
Intravenous Morphine

Background Previous studies have shown that genetic variability at position 118 of the human mu-opioid receptor gene altered patients' response to intravenous morphine. The purpose of this study was to investigate whether this polymorphism contributes to the variability in response to morphine for postcesarean analgesia. Methods After investigators obtained informed consent, 588 healthy women received 0.1 mg intrathecal morphine for postcesarean analgesia. Their blood samples were genotyped for the A118G polymorphism-A118 homozygous (AA), heterozygous (AG), or homozygous for the G allele (GG). Pain scores, the severity of nausea and vomiting, the incidence of pruritus, and the total self-administered intravenous morphine were recorded for the first 24 postoperative hours. Results Two hundred seventy women (46%) were AA, 234 (40%) were AG, and 82 (14%) were GG. The 24-h self-administered intravenous morphine consumption was lowest in the AA group (P = 0.001; mean, 5.9; 95% confidence interval, 5.1-6.8) versus the AG (8.0; 6.9-9.1) and GG groups (9.4; 7.3-11.5). Pain scores were lowest in the AA group and highest in the GG group, with a statistically significant difference detected between AA, AG, and GG (P = 0.049). Total morphine consumption was also influenced by patients' age and paying status. AA group was associated with the highest incidence of nausea (26 of 272 [9.6%]; P = 0.02) versus the other two groups (13 of 234 [5.6%] and 1 of 82 [1.2%] for AG and GG, respectively). Conclusion Genetic variation at position 118 of the mu-opioid receptor is associated with interindividual differences in pain scores, self-administered intravenous morphine, and the incidence of nausea postoperatively.

Mu Opioid Receptor Gene (OPRM1) in Patients With Opiate Use Disorder

2020 ◽  
Vol 19 (1) ◽  
pp. 16-21
Author(s):  
Nehal Mostafa ◽  
Maha W. Mobasher ◽  
Heba N. El Baz ◽  
Mohamed A. Khalil
Keyword(s):  
Opioid Receptor ◽  
Receptor Gene ◽  
Mu Opioid Receptor ◽  
Mu Opioid ◽  
Opiate Use ◽  
Opiate Use Disorder

scholarly journals Deletion of the mu opioid receptor gene in mice reshapes the reward–aversion connectome

2016 ◽  
Vol 113 (41) ◽  
pp. 11603-11608 ◽  
Author(s):  
Anna E. Mechling ◽  
Tanzil Arefin ◽  
Hsu-Lei Lee ◽  
Thomas Bienert ◽  
Marco Reisert ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Opioid Receptor ◽  
Resting State ◽  
Receptor Gene ◽  
Resting State Fmri ◽  
Mu Opioid Receptor ◽  
Major Influence ◽  
Mu Opioid ◽  
Brain Connectome ◽  
Intergroup Comparison

Connectome genetics seeks to uncover how genetic factors shape brain functional connectivity; however, the causal impact of a single gene’s activity on whole-brain networks remains unknown. We tested whether the sole targeted deletion of the mu opioid receptor gene (Oprm1) alters the brain connectome in living mice. Hypothesis-free analysis of combined resting-state fMRI diffusion tractography showed pronounced modifications of functional connectivity with only minor changes in structural pathways. Fine-grained resting-state fMRI mapping, graph theory, and intergroup comparison revealed Oprm1-specific hubs and captured a unique Oprm1 gene-to-network signature. Strongest perturbations occurred in connectional patterns of pain/aversion-related nodes, including the mu receptor-enriched habenula node. Our data demonstrate that the main receptor for morphine predominantly shapes the so-called reward/aversion circuitry, with major influence on negative affect centers.

scholarly journals Single-nucleotide polymorphism in the human mu opioid receptor gene alters β-endorphin binding and activity: Possible implications for opiate addiction

1998 ◽  
Vol 95 (16) ◽  
pp. 9608-9613 ◽  
Author(s):  
Cherie Bond ◽  
K. Steven LaForge ◽  
Mingting Tian ◽  
Dorothy Melia ◽  
Shengwen Zhang ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Methadone Maintenance ◽  
Receptor Gene ◽  
Mu Opioid Receptor ◽  
Coding Region ◽  
Allelic Form ◽  
Endogenous Opioid ◽  
Single Nucleotide ◽  
Allele Distribution ◽  
Mu Opioid

Opioid drugs play important roles in the clinical management of pain, as well as in the development and treatment of drug abuse. The mu opioid receptor is the primary site of action for the most commonly used opioids, including morphine, heroin, fentanyl, and methadone. By sequencing DNA from 113 former heroin addicts in methadone maintenance and 39 individuals with no history of drug or alcohol abuse or dependence, we have identified five different single-nucleotide polymorphisms (SNPs) in the coding region of the mu opioid receptor gene. The most prevalent SNP is a nucleotide substitution at position 118 (A118G), predicting an amino acid change at a putative N-glycosylation site. This SNP displays an allelic frequency of approximately 10% in our study population. Significant differences in allele distribution were observed among ethnic groups studied. The variant receptor resulting from the A118G SNP did not show altered binding affinities for most opioid peptides and alkaloids tested. However, the A118G variant receptor binds β-endorphin, an endogenous opioid that activates the mu opioid receptor, approximately three times more tightly than the most common allelic form of the receptor. Furthermore, β-endorphin is approximately three times more potent at the A118G variant receptor than at the most common allelic form in agonist-induced activation of G protein-coupled potassium channels. These results show that SNPs in the mu opioid receptor gene can alter binding and signal transduction in the resulting receptor and may have implications for normal physiology, therapeutics, and vulnerability to develop or protection from diverse diseases including the addictive diseases.

scholarly journals Isolation and characterization of new exon 11-associated N-terminal splice variants of the human mu opioid receptor gene

2009 ◽  
Vol 108 (4) ◽  
pp. 962-972 ◽  
Author(s):  
Jin Xu ◽  
Mingming Xu ◽  
Yasmin L. Hurd ◽  
Gavril W. Pasternak ◽  
Ying-Xian Pan
Keyword(s):  
Opioid Receptor ◽  
Splice Variants ◽  
Receptor Gene ◽  
Mu Opioid Receptor ◽  
Mu Opioid ◽  
Isolation And Characterization ◽  
Exon 11

The histidine triad nucleotide-binding protein 1 supports mu-opioid receptor–glutamate NMDA receptor cross-regulation

2010 ◽  
Vol 68 (17) ◽  
pp. 2933-2949 ◽  
Author(s):  
María Rodríguez-Muñoz ◽  
Pilar Sánchez-Blázquez ◽  
Ana Vicente-Sánchez ◽  
Concha Bailón ◽  
Beatriz Martín-Aznar ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Opioid Receptor ◽  
Binding Protein ◽  
Nucleotide Binding ◽  
Mu Opioid Receptor ◽  
Mu Opioid ◽  
Nucleotide Binding Protein

Social hedonic capacity is associated with the A118G polymorphism of the mu-opioid receptor gene (OPRM1) in adult healthy volunteers and psychiatric patients

2011 ◽  
Vol 6 (1) ◽  
pp. 88-97 ◽  
Author(s):  
Alfonso Troisi ◽  
Giovanni Frazzetto ◽  
Valeria Carola ◽  
Giorgio Di Lorenzo ◽  
Mariangela Coviello ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Opioid Receptor ◽  
Psychiatric Patients ◽  
Receptor Gene ◽  
Mu Opioid Receptor ◽  
Mu Opioid ◽  
Hedonic Capacity ◽  
A118g Polymorphism

Association of Alcohol or Other Drug Dependence with Alleles of the mu Opioid Receptor Gene (OPRM1)

1998 ◽  
Vol 22 (6) ◽  
pp. 1359-1362 ◽  
Author(s):  
Henry R. Kranzler ◽  
Joel Gelernter ◽  
Stephanie O'Malley ◽  
Carlos A. Hernandez-Avila ◽  
Daniel Kaufman
Keyword(s):  
Opioid Receptor ◽  
Drug Dependence ◽  
Receptor Gene ◽  
Mu Opioid Receptor ◽  
Mu Opioid
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