Intact risk-based decision making in rats with prefrontal or accumbens dopamine depletion

Abstract

The medial prefrontal cortex (mPFC) and the core region of the nucleus accumbens (AcbC) are key regions of a neural system that subserves risk-based decision making. Here, we examined whether dopamine (DA) signals conveyed to the mPFC and AcbC are critical for risk-based decision making. Rats with 6-hydroxydopamine or vehicle infusions into the mPFC or AcbC were examined in an instrumental task demanding probabilistic choice. In each session, probabilities of reward delivery after pressing one of two available levers were signaled in advance in forced trials followed by choice trials that assessed the animal's preference. The probabilities of reward delivery associated with the large/risky lever declined systematically across four consecutive blocks but were kept constant within four subsequent daily sessions of a particular block. Thus, in a given session, rats need to assess the current value associated with the large/risky versus small/certain lever and adapt their lever preference accordingly. Results demonstrate that the assessment of within-session reward probabilities and probability discounting across blocks were not altered in rats with mPFC and AcbC DA depletions, relative to sham controls. These findings suggest that the capacity to evaluate the magnitude and likelihood of rewards associated with alternative courses of action seems not to rely on intact DA transmission in the mPFC or AcbC.

Hippocampal interplay with the nucleus accumbens is critical for decisions about time

“…At the same time, studies that have explicitly examined the role of dopamine levels in experiments involving time trade‐offs have failed to find that such dysregulation impacts decision‐making. For example, it has been shown that depletion of local dopamine levels in the NAc does not affect time‐discounting judgments in decision‐making tasks (Winstanley et al ., ) and nor does it affect decision‐making in other settings (Walton et al ., ; see also Mai & Hauber, ). This finding is difficult to reconcile with the proposition that the critical role of vHC/NAc interaction in the deficits that we observed is in the regulation of dopamine.…”

“…The first five sessions ensured that the rats learned the response–outcome contingency at a given probability through experience. This experience occurred through a high number of ‘forced choice’ trials for each probability (30 in total, 15 per stimulus; see ), so that the animal could accurately estimate the probability of reward given its infrequent occurrence (see also, Mobini et al ., ; Nasrallah et al ., , ; Mai & Hauber, ). Thus, unlike previous studies that include few forced choice trials irrespective of probability (e.g.…”

“…Instead, we allowed choice behavior to stabilise at one probability before moving onto the next. This ensured that the rat received sufficient exposure to the contingencies so that it could accurately estimate the probability of reward given its infrequent occurrence (see also Mobini et al ., ; Nasrallah et al ., , ; Mai & Hauber, ). Our design also prevents the potential effect of satiation leading to a shift in the animal's motivational state (Mai et al ., ).…”

Intersection of effort and risk: ethological and neurobiological perspectives

“…Furthermore, infusion of D1 antagonists into the NAC of rats decreases the preference for larger, uncertain rewards on a probability discounting task. In contrast, infusion of a D1 or D2/D3 agonists into the NAC i ncreases risk preference when reward probability is high (Norbury et al, 2013; Stopper et al, 2013; however, see Mai and Hauber, 2012). Infusion of D1 agonists into the NAC may also “optimize” decision making in treated animals as one study reported that treated rats were more likely to choose the large and uncertain reward when reward probability was high, but were more likely to avoid this option when probabilities were low (Stopper et al, 2013).…”

“…Furthermore, increases in dopamine concentration are associated with increased risk preference in humans (Zack and Poulos, 2004; Dodd et al, 2005; Dang et al, 2011) and rodents (St. Onge and Floresco, 2009; Stopper et al, 2013). Finally, stimulation of dopamine D1 receptors within the NAC enhances risk preference (Stopper et al, 2013; however, see Mai and Hauber, 2012). Consequently, we propose that effort-induced increases in NAC dopamine concentration drives risk preference by enhancing dopamine release in the NAC.…”