Nucleus accumbens DRD2 receptor agonism attenuates escape behavior.

Animals learn to approach and escape stimuli in their environment, in part through the representation of rewarding or aversive outcomes in the nucleus accumbens (NAc). The regulation of reward motivation in the NAc by dopamine signaling at DRD1 and DRD2 receptors has been the subject of extensive study. However, the process by which aversive stimuli are signaled within this system to promote motivated escape behavior is less well characterized. Conventional wisdom posits that rewarding and aversive stimuli ultimately affect DRD1 or DRD2-receptor expressing medium spiny neurons (MSNs) in an opposing manner to differentially modulate motivated behavior. However, recent studies have challenged this view and demonstrate the need to better characterize the processes that mediate aversion learning. To determine if DRD2 dopamine receptor activation disrupts escape behavior, 21 male and female Sprague Dawley rats were treated with an intra-NAc core DRD2 receptor agonist, quinpirole, while escape behavior was negatively reinforced by the termination of aversive white noise. This treatment attenuated escape, a result that is consistent with the view that aversion-induced reductions in dopamine promote escape behavior through decreased DRD2 receptor signaling in the NAc, and potential disinhibition of an aversion-sensitive striatal output circuit.