RESUMO
Acute stress has been shown to influence reward sensitivity, feedback learning, and risk-taking during decision-making, primarily through activation of the hypothalamic pituitary axis (HPA). However, it is unclear how acute stress affects decision-making among choices that vary in their degree of uncertainty. To address this question, we conducted two experiments in which participants repeatedly chose between two options-a high-uncertainty option that offered highly variable rewards but was advantageous in the long-term, and a low-uncertainty option that offered smaller yet more consistent rewards. The Socially Evaluated Cold Pressor Task (SECPT) was utilized to induce acute stress. Participants in Experiment 1 (N = 114) were exposed to either the SECPT or a warm-water control condition and then completed the decision-making under uncertainty task. Compared to the control condition, those exposed to the acute stress manipulation chose the high-uncertainty option that provided highly variable but larger rewards over the option that provided stable, smaller rewards. Experiment 2 (N = 95) incorporated a salivary cortisol measure. Results replicated the behavioral findings in Experiment 1 and demonstrated that the acute stress manipulation increased salivary cortisol. This work suggests that moderate acute stress is associated with tolerance of outcome variability in contexts that depend on learning to maximize rewards.
Assuntos
Tomada de Decisões , Recompensa , Humanos , Hidrocortisona , IncertezaRESUMO
Variability in valacyclovir bioavailability and the potential for cephalexin-valacyclovir interaction were evaluated. The intraindividual acyclovir area under the concentration-time curve (AUC) varied minimally, whereas interindividual differences were substantial. Coadministration of the human peptide transporter 1 (hPEPT1) substrates valacyclovir and cephalexin minimally reduced the acyclovir AUC. These results suggest a stable valacyclovir absorption phenotype, significant interindividual variability, and minimal interaction between these hPEPT1 substrates.