Disruptions in effort-based decision-making and consummatory behavior following antagonism of the dopamine D2 receptor

• Published in: Behavioural brain research Vol. 320; pp. 431 - 439
• Main Authors: Robles, Cindee F., Johnson, Alexander W.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.03.2017
• Subjects: Analysis of Variance; Animals; Conditioning, Operant - drug effects; Conditioning, Operant - physiology; Consummatory Behavior - drug effects; Consummatory Behavior - physiology; Decision Making - drug effects; Decision Making - physiology; Dopamine Antagonists - pharmacology; Dose-Response Relationship, Drug; Effort discounting; Feeding Behavior - drug effects; Hedonic; Incentive; Mesocorticolimbic; Mesostriatal; Mice; Motivation - drug effects; Motivation - physiology; Receptors, Dopamine D2 - metabolism; Reinforcement Schedule; Salicylamides - pharmacology; Incentive; Mesostriatal; Effort discounting; Hedonic; Mesocorticolimbic
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2016.10.043

•Dopamine is known to influence motivational processes.•Disruptions in dopamine D2 receptor signaling on reward-based decision-making and consummatory behavior were studied.•In mice, central infusion of D2 antagonist eticlopride impaired effort-based decision-making.•Eticopride also attenuated sucrose consumption by reducing motivation to consume.•Results suggest eticlopride reduced the willingness to engage in effortful operant responding and consumption of sucrose. Dopamine is known to influence motivational processes, however the precise role of this neurotransmitter remains a contentious issue. In the current study we sought to further characterize dopamine signaling in reward-based decision-making and consummatory behavior in mice, via lateral ventricle infusion of the dopamine D2 receptor antagonist eticlopride. In Experiment 1, we examined effort-based decision-making, in which mice had a choice between one lever, where a single response led to the delivery of a low value reward (2% sucrose); and a second lever, which led to a higher value reward (20% sucrose) that gradually required more effort to obtain. As the response schedule for the high value reward became more strict, low dose (4μg in 0.5μl) central infusions of eticlopride biased preference away from the high value reward, and toward the lever that led to the low value reward. Similarly, a higher dose of eticlopride (8μg in 0.5μl) also disrupted choice responding for the high value reward, however it did so by increasing omissions. In Experiment 2, we assessed the effects of eticlopride on consumption of 20% sucrose. The antagonist led to a dose-dependent reduction in intake, and through an analysis of licking microstructure, it was revealed that this in part reflected a reduction in the motivation to engage in consummatory behavior, rather than alterations in the evaluation of the reward. These results suggest that disruptions in D2 receptor signaling reduce the willingness to engage in effortful operant responding and consumption of a desirable outcome.