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 ◽  
...  
2011 ◽  
Vol 26 (S2) ◽  
pp. 2055-2055
Author(s):  
A. Troisi

IntroductionMost of us find social encounters rewarding, especially when we encounter those with whom we are familiar and have built up a relationship. From an evolutionary point of view, this is not surprising considering that human beings are fundamentally social organisms. Considering that endogenous opioids mediate hedonic responses to a variety of natural rewards, the common A118G polymorphism in the mu-opioid receptor gene (OPRM1) might also modulate individual differences in the capacity to experience social reward.AimsIn the present study, we hypothesized that, compared to individuals with the A118A genotype, individuals expressing the minor 118G allele had an increased need for affiliation and an increased capacity to experience social reward.MethodsIn a mixed sample (N = 214) of adult healthy volunteers and psychiatric patients, we analyzed the association between the A118G polymorphism of the OPRM1 and two different psychological constructs reflecting individual differences in the capacity to experience social reward.ResultsCompared to individuals expressing only the major allele (A) of the A118G polymorphism, subjects expressing the minor allele (G) had an increased tendency to become engaged in affectionate relationships, as indicated by lower scores on a self-report measure of avoidant attachment, and experienced more pleasure in social situations, as indicated by lower scores on a self-report measure of social anhedonia.ConclusionsThe results reported here are in agreement with the brain opioid hypothesis of social attachment and raise several questions about the maintenance of the A118G polymorphism in the evolution of human social behavior.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Alan M. Daniel ◽  
Brenda G. Rushing ◽  
Karla Y. Tapia Menchaca

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.


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 ◽  
...  

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.


2020 ◽  
Vol 19 (1) ◽  
pp. 16-21
Author(s):  
Nehal Mostafa ◽  
Maha W. Mobasher ◽  
Heba N. El Baz ◽  
Mohamed A. Khalil

2016 ◽  
Vol 113 (41) ◽  
pp. 11603-11608 ◽  
Author(s):  
Anna E. Mechling ◽  
Tanzil Arefin ◽  
Hsu-Lei Lee ◽  
Thomas Bienert ◽  
Marco Reisert ◽  
...  

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.


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