Dispositional greed, characterized by the insatiable hunger for more and the dissatisfaction for not having enough, has often been associated with heightened impulsivity and excessive risk-taking. Despite its far-reaching implications in social science and economics, however, the exact neural mechanisms of how greed personality influences risk-taking are still ill understood. In the present study, we showed the correlation between subjects' greed personality trait (GPT) scores and risk-taking was selectively mediated by individual's loss aversion, but not risk attitude. In addition, our neuroimaging results indicated that gain and loss prospects were jointly represented in the activities of the ventral striatum and medial orbitofrontal cortex (mOFC). Furthermore, mOFC responses also encoded the neural loss aversion signal and mediated the association between individual differences in GPT scores and behavioral loss aversion. Our findings provide a basis for understanding the specific neural mechanisms that mediates the effect of greed personality trait on risk-taking behaviors.
All data generated or analysed during this study are included in the manuscript and supporting files. Source data files have been provided in https://osf.io/rpve7/
Neural mediation of greed personality trait on economic risk-takingOpen Science Framework, doi: 10.17605/OSF.IO/RPVE7.
- Jian Li
- Jian Li
- Jian Li
The funders had no role in study design, data collection, and interpretation, or the decision to submit the work for publication.
Human subjects: Human subjects: All participants provided written informed consent. Study procedures were reviewed and approved by the Ethics Committee at Peking University (2017-11-01).
- Thorsten Kahnt, Northwestern University Feinberg School of Medicine, United States
© 2019, Li et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Several discrete groups of feeding-regulated neurons in the nucleus of the solitary tract (nucleus tractus solitarius; NTS) suppress food intake, including avoidance-promoting neurons that express Cck (NTSCck cells) and distinct Lepr- and Calcr-expressing neurons (NTSLepr and NTSCalcr cells, respectively) that suppress food intake without promoting avoidance. To test potential synergies among these cell groups we manipulated multiple NTS cell populations simultaneously. We found that activating multiple sets of NTS neurons (e.g., NTSLepr plus NTSCalcr (NTSLC), or NTSLC plus NTSCck (NTSLCK)) suppressed feeding more robustly than activating single populations. While activating groups of cells that include NTSCck neurons promoted conditioned taste avoidance (CTA), NTSLC activation produced no CTA despite abrogating feeding. Thus, the ability to promote CTA formation represents a dominant effect but activating multiple non-aversive populations augments the suppression of food intake without provoking avoidance. Furthermore, silencing multiple NTS neuron groups augmented food intake and body weight to a greater extent than silencing single populations, consistent with the notion that each of these NTS neuron populations plays crucial and cumulative roles in the control of energy balance. We found that silencing NTSLCK neurons failed to blunt the weight-loss response to vertical sleeve gastrectomy (VSG) and that feeding activated many non-NTSLCK neurons, however, suggesting that as-yet undefined NTS cell types must make additional contributions to the restraint of feeding.
In the fruit fly Drosophila melanogaster, gustatory sensory neurons express taste receptors that are tuned to distinct groups of chemicals, thereby activating neural ensembles that elicit either feeding or avoidance behavior. Members of a family of ligand -gated receptor channels, the Gustatory receptors (Grs), play a central role in these behaviors. In general, closely related, evolutionarily conserved Gr proteins are co-expressed in the same type of taste neurons, tuned to chemically related compounds, and therefore triggering the same behavioral response. Here, we report that members of the Gr28 subfamily are expressed in largely non-overlapping sets of taste neurons in Drosophila larvae, detect chemicals of different valence, and trigger opposing feeding behaviors. We determined the intrinsic properties of Gr28 neurons by expressing the mammalian Vanilloid Receptor 1 (VR1), which is activated by capsaicin, a chemical to which wild-type Drosophila larvae do not respond. When VR1 is expressed in Gr28a neurons, larvae become attracted to capsaicin, consistent with reports showing that Gr28a itself encodes a receptor for nutritious RNA. In contrast, expression of VR1 in two pairs of Gr28b.c neurons triggers avoidance to capsaicin. Moreover, neuronal inactivation experiments show that the Gr28b.c neurons are necessary for avoidance of several bitter compounds. Lastly, behavioral experiments of Gr28 deficient larvae and live Ca2+ imaging studies of Gr28b.c neurons revealed that denatonium benzoate, a synthetic bitter compound that shares structural similarities with natural bitter chemicals, is a ligand for a receptor complex containing a Gr28b.c or Gr28b.a subunit. Thus, the Gr28 proteins, which have been evolutionarily conserved over 260 million years in insects, represent the first taste receptor subfamily in which specific members mediate behavior with opposite valence.