RATIONALE: Nicotine (NIC) administration can increase behaviors that result in delivery of non-drug reinforcers (e.g., salient sensory stimuli). However, little is known about the circumstances under which NIC increases these behaviors. OBJECTIVE: The present studies sought to extend the reinforcement enhancing effects of NIC to sucrose rewards for which intensity could be systematically manipulated. METHOD: In Experiment 1, rats were trained to respond for sucrose (30% w/v) on a progressive ratio (PR) schedule of reinforcement and were pretreated with NIC (0.4 mg/kg free-base) or physiological saline (SAL). The intensity of the sucrose reward was manipulated over subsequent testing sessions (0-60% w/v). Similar procedures were used in Experiment 2; however, each subject received only one sucrose concentration (0-20%) to control for conditioning history. In Experiment 3, a fixed ratio 3 (FR3) schedule of reinforcement was used to investigate putative activating effects of NIC. Experiment 4 investigated whether NIC pretreatment would reduce sucrose intake in limited-access drinks. RESULTS: In Experiment 1, NIC increased the motivation to obtain all sucrose concentrations, including water. However, when conditioning history was controlled (Experiment 2) the reinforcement enhancing effects of NIC were systematically related to the strength of the reinforcer. In Experiment 3, NIC neither increased nor decreased responding for sucrose. In Experiment 4, NIC reduced sucrose intake, but only at concentrations that resulted in peak drink volumes (5-20%). CONCLUSION: The results suggest that the reinforcement enhancing effects of NIC depend on conditioning history and do not appear to be the result of simple behavioral activation.
RATIONALE: Nicotine (NIC) administration can increase behaviors that result in delivery of non-drug reinforcers (e.g., salient sensory stimuli). However, little is known about the circumstances under which NIC increases these behaviors. OBJECTIVE: The present studies sought to extend the reinforcement enhancing effects of NIC to sucrose rewards for which intensity could be systematically manipulated. METHOD: In Experiment 1, rats were trained to respond for sucrose (30% w/v) on a progressive ratio (PR) schedule of reinforcement and were pretreated with NIC (0.4 mg/kg free-base) or physiological saline (SAL). The intensity of the sucrose reward was manipulated over subsequent testing sessions (0-60% w/v). Similar procedures were used in Experiment 2; however, each subject received only one sucrose concentration (0-20%) to control for conditioning history. In Experiment 3, a fixed ratio 3 (FR3) schedule of reinforcement was used to investigate putative activating effects of NIC. Experiment 4 investigated whether NIC pretreatment would reduce sucrose intake in limited-access drinks. RESULTS: In Experiment 1, NIC increased the motivation to obtain all sucrose concentrations, including water. However, when conditioning history was controlled (Experiment 2) the reinforcement enhancing effects of NIC were systematically related to the strength of the reinforcer. In Experiment 3, NIC neither increased nor decreased responding for sucrose. In Experiment 4, NIC reduced sucrose intake, but only at concentrations that resulted in peak drink volumes (5-20%). CONCLUSION: The results suggest that the reinforcement enhancing effects of NIC depend on conditioning history and do not appear to be the result of simple behavioral activation.
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