Enhanced risky choice in male rats elicited by the acute pharmacological stressor yohimbine involves prefrontal dopamine D1 receptor activation.

BACKGROUND: Acute stress alters risk-based decision making, however, the underlying neural and neurochemical substrates are underexplored. Given their well-documented stress-inducing effects in humans and laboratory animals, glucocorticoids such as cortisol and corticosterone and the α2-adrenoceptor antagonist yohimbine represent potent pharmacological tools to mimic some characteristics of acute stress.

METHODS: Here, we analyzed the effects of the pharmacological stressors corticosterone and yohimbine given systemically on risk-based decision making in male rats. Moreover, we investigated whether pharmacological stressor effects on risk-based decision making involve dopamine D1 receptor stimulation in the dorsal prelimbic cortex (PL). We used a risk discounting task that requires choosing between a certain/small reward lever that always delivered one pellet and a risky/large reward lever which delivered four pellets with a decreasing probability across subsequent trials.

RESULTS: Systemic administration of yohimbine increased the preference for the risky/large reward lever. By contrast, systemic single administration of corticosterone did not significantly promote risky choice. Moreover, co-administration of corticosterone did not enhance the effects of yohimbine on risky choice. The data further show that the increased preference for the risky/large reward lever under systemic yohimbine was lowered by a concurrent pharmacological blockade of dopamine D1 receptors in the PL.

CONCLUSIONS: Our rodent data provide causal evidence that stimulation of PL D1 receptors may represent a neurochemical mechanism by which the acute pharmacological stressor yohimbine, and possibly non-pharmacological stressors as well, promote risky choice.