• Individual differences in decision making: Drive and reward responsiveness affect strategic bargaining in economic games

      Scheres, Anouk; Sanfey, Alan; Psychology Department, University of Arizona, 1503 E University Blvd., Tucson AZ 85721, USA (BioMed Central, 2006)
      BACKGROUND:In the growing body of literature on economic decision making, the main focus has typically been on explaining aggregate behavior, with little interest in individual differences despite considerable between-subject variability in decision responses. In this study, we were interested in asking to what degree individual differences in fundamental psychological processes can mediate economic decision-making behavior.METHODS:Specifically, we studied a personality dimension that may influence economic decision-making, the Behavioral Activation System, (BAS) which is composed of three components: Reward Responsiveness, Drive, and Fun Seeking. In order to assess economic decision making, we utilized two commonly-used tasks, the Ultimatum Game and Dictator Game. Individual differences in BAS were measured by completion of the BIS/BAS Scales, and correlations between the BAS scales and monetary offers made in the two tasks were computed.RESULTS:We found that higher scores on BAS Drive and on BAS Reward Responsiveness were associated with a pattern of higher offers on the Ultimatum Game, lower offers on the Dictator Game, and a correspondingly larger discrepancy between Ultimatum Game and Dictator Game offers.CONCLUSION:These findings are consistent with an interpretation that high scores on Drive and Reward Responsiveness are associated with a strategy that first seeks to maximize the likelihood of reward, and then to maximize the amount of reward. More generally, these results suggest that there are additional factors other than empathy, fairness and selfishness that contribute to strategic decision-making.
    • Midazolam, hippocampal function, and transitive inference: Reply to Greene

      Frank, Michael; O'Reilly, Randall; Curran, Tim; Dept of Psychology and Program in Neuroscience, University of Arizona, Tucson, USA; Dept of Psychology and Center for Neuroscience, University of Colorado at Boulder. Boulder, USA (BioMed Central, 2008)
      The transitive inference (TI) task assesses the ability to generalize learned knowledge to new contexts, and is thought to depend on the hippocampus (Dusek & Eichenbaum, 1997). Animals or humans learn in separate trials to choose stimulus A over B, B over C, C over D and D over E, via reinforcement feedback. Transitive responding based on the hierarchical structure A > B > C > D > E is then tested with the novel BD pair. We and others have argued that successful BD performance by animals - and even humans in some implicit studies - can be explained by simple reinforcement learning processes which do not depend critically on the hippocampus, but rather on the striatal dopamine system. We recently showed that the benzodiazepene midazolam, which is thought to disrupt hippocampal function, profoundly impaired human memory recall performance but actually enhanced implicit TI performance (Frank, O'Reilly & Curran, 2006). We posited that midazolam biased participants to recruit striatum during learning due to dysfunctional hippocampal processing, and that this change actually supported generalization of reinforcement values. Greene (2007) questions the validity of our pharmacological assumptions and argues that our conclusions are unfounded. Here we stand by our original hypothesis, which remains the most parsimonious account of the data, and is grounded by multiple lines of evidence.
    • Number of risk genotypes is a risk factor for major depressive disorder: a case control study

      Garriock, Holly; Delgado, Pedro; Kling, Mitchel; Carpenter, Linda; Burke, Michael; Burke, William; Schwartz, Thomas; Marangell, Lauren; Husain, Mustafa; Erickson, Robert; et al. (BioMed Central, 2006)
      BACKGROUND:The objective of the study was to determine the genetic basis of Major Depressive Disorder, and the capacity to respond to antidepressant treatment. An association study of 21 candidate polymorphisms relevant to monoamine function and the mechanism of antidepressant response was conducted in 3 phenotypically distinct samples: a group with chronic or recurrent depression unable to respond to antidepressants (non-responders) (n = 58), a group capable of symptomatic improvement with or without treatment (responders) (n = 39), and volunteer controls (n = 85). The responders and non-responders constituted a larger group of depressed subjects.METHODS:A candidate gene approach was employed to asses the genetics basis of Major Depressive Disorder. The genotypic frequencies of selected polymorphisms were compared between the controls and depressed subjects. To asses the genetics basis of the capacity to respond to antidepressant treatment, the responders were compared to the non-responders. Candidate genes were chosen based on functional studies and proximity to whole genome linkage findings in the literature. Risk genotypes were identified by previous functional studies and association studies.RESULTS:A statistically significant difference in genotype frequency for the SLC6A4 intron 2 VNTR was detected between the subjects with a history of depression and controls (p = 0.004). Surprisingly, a statistically significant difference was detected between responders and non-responders for the DRD4 exon III VNTR genotype frequencies (p = 0.009). Furthermore, a difference between the controls and depressed subjects as well as between the controls and non-responders was detected for the number and distribution of risk genotypes in each group.CONCLUSION:An association between several monoamine-related genes and Major Depressive Disorder is supported. The data suggest that the two depressive phenotypes are genetically different, inferring that the genetic basis for the capacity to respond to standard antidepressant treatment, and the genetic susceptibility to Major Depressive Disorder may be independent. In addition, a proof of concept is provided demonstrating that the number of risk genotypes may be an indication of susceptibility of major depressive disorder and the severity of the disorder.