Interaction of CCKB receptors with amphetamine in responding for conditioned rewards

Cholecystokinin (CCK) has been localized in the nucleus accumbens (NAC) where it may interact with dopamine neurotransmission. NAC dopamine is involved in the control over behavior produced by conditioned rewards. The present experiment tested the whether blockade of endogenous CCKB receptors with L-365,260 (0.1 mg/kg, IP) potentiates bar pressing for stimuli previously associated with food reward. Intra-accumbens amphetamine (20 micrograms) facilitated bar pressing for conditioned rewards. Systemic administration of L-365,260 potentiated this amphetamine response but produced no effect on responding when administered alone. These findings suggest that endogenous CCKB mechanisms may normally inhibit DA function in reward-related behaviors.