The dopamine D2 antagonist eticlopride accelerates extinction and delays reacquisition of food self-administration in rats.

Dopamine receptors are implicated in the reinforcing effects of food and drug reinforcement. The purpose of this study was to evaluate whether blocking D2 dopamine receptors during extinction (secondary reinforcement) would affect reacquisition of responding for food pellets (primary reinforcement). Food-restricted rats self-administered (fixed-ratio 1) food pellets in 1-h daily sessions for 7 days. For the next 7 days rats responded in extinction conditions. Before each extinction session rats were injected with saline or the dopamine D2 antagonist eticlopride (0.03 mg/kg, subcutaneously). After the extinction phase, rats were allowed to reacquire food pellet self-administration in seven daily sessions, and received saline or eticlopride before each session. Four treatment groups were represented: saline extinction, saline reacquisition; eticlopride extinction, saline reacquisition; saline extinction, eticlopride reacquisition; and eticlopride extinction, eticlopride reacquisition. Locomotor activity did not differ between eticlopride-treated and saline-treated rats throughout the study. Extinction was accelerated in eticlopride-treated rats. Eticlopride also delayed reacquisition of food self-administration compared with saline-treated rats. Rats administered eticlopride during extinction showed delayed reacquisition and a decreased response rate for food during the reacquisition phase. Indirectly reducing the value of a reinforcer in this way may provide a novel approach for reducing addiction-related food or drug self-administration behaviors.