Abstract

Corticosteroid hormones, released after stress, are known to influence neuronal activity and produce a wide range of effects upon the brain. They affect cognitive tasks including decision-making. Recently it was shown that systemic injections of corticosterone (CORT) disrupt reward-based decision-making in rats when tested in a rat model of the Iowa Gambling Task (rIGT), i.e., rats do not learn across trial blocks to avoid the long-term disadvantageous option. This effect was associated with a change in neuronal activity in prefrontal brain areas, i.e., the infralimbic (IL), lateral orbitofrontal (lOFC) and insular cortex, as assessed by changes in c-Fos expression. Here, we studied whether injections of CORT directly into the IL and lOFC lead to similar changes in decision-making. As in our earlier study, CORT was injected during the final 3 days of the behavioral paradigm, 25 min prior to behavioral testing. Infusions of vehicle into the IL led to a decreased number of visits to the disadvantageous arm across trial blocks, while infusion with CORT did not. Infusions into the lOFC did not lead to differences in the number of visits to the disadvantageous arm between vehicle treated and CORT treated rats. However, compared to vehicle treated rats of the IL group, performance of vehicle treated rats of the lOFC group was impaired, possibly due to cannulation/infusion-related damage of the lOFC affecting decision-making. Overall, these results show that infusions with CORT into the IL are sufficient to disrupt decision-making performance, pointing to a critical role of the IL in corticosteroid effects on reward-based decision-making. The data do not directly support that the same holds true for infusions into the lOFC.

Highlights

  • Stress is the subjective experience of actual or potential, physical or psychological threat

  • We found impaired decision-making of male rats tested 30 min after systemic injections of CORT (1 mg/kg subcutaneously): unlike vehicle treated rats, CORT treated rats did not decrease their number of visits to the disadvantageous arm across trial blocks (Koot et al, 2013)

  • In the IL-infused group, 12 additional rats were excluded; 5 due to incorrect placement of the cannulas, 1 due to loss of 1 guide cannula, 1 because the target region of the cannulas was impossible to verify, 2 due to large infections in the brain, 2 due to not completing the rodent version of the IGT (rIGT) and 1 due to health problems affecting the performance. This resulted in n = 34 rats used for the analysis (CORT = 21, vehicle = 13)

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Summary

Introduction

Stress is the subjective experience of actual or potential, physical or psychological threat. As part of the stress response, the adrenal cortex secretes glucocorticosteroid hormones in response to adrenocorticotropic hormone from the pituitary gland. Neurons may receive high levels of corticosteroids (cortisol in humans, corticosterone (CORT) in most rodents), which influence neuronal activity and produce a wide range of effects upon the brain (McEwen, 2006; Groeneweg et al, 2011). Altered gene transcription mediates many of the glucocorticoid actions, but a range of effects on behavior and endocrine output occurs within minutes (Groeneweg et al, 2011). Glucocorticosteroids restore homeostasis in the aftermath of stress by diverting energy supply to challenged tissues and control the excitability of neuronal networks (de Kloet et al, 1999)

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