The generality of nicotine as a reinforcer enhancer in rats: effects on responding maintained by primary and conditioned reinforcers and resistance to extinction
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Nicotine may enhance the reinforcing value of other reinforcers. It is unclear whether nicotine enhances responding maintained by all reinforcers or whether there are limits to this role.
The objective of the study is to test the generality of nicotine-induced increases in reinforced responding by using an observing response procedure, which generated measures of responding maintained by food reinforcers, conditioned reinforcers, and responding during extinction. We also examined whether nicotine increased resistance to extinction and whether nicotine’s effects could be characterized as rate-dependent.
Materials and methods
Rats received presession subcutaneous injections of Vehicle (n = 5), 0.3 (n = 6), or 0.56 (n = 6) mg/kg nicotine for 70 sessions. Resistance to extinction was also assessed by removing food for five sessions.
Nicotine did not consistently affect food or extinction responding. Both doses of nicotine produced increases in responding maintained by conditioned reinforcers, but did not increase resistance to extinction. Predrug response rates accounted for a small but significant percentage of the variance in the drug effect.
Although there was a tendency for nicotine to increase low predrug response rates (i.e., response rates just prior to nicotine administration), 0.3 and 0.56 mg/kg nicotine systematically increased responding maintained by conditioned reinforcers. The results are consistent with a reinforcer-enhancing role of nicotine. However, nicotine did not increase resistance to extinction, nor did it increase food-maintained responses. Nicotine may selectively increase responding maintained by moderately reinforcing stimuli, such as the conditioned reinforcers used in the present study.
KeywordsNicotine Observing response procedure Resistance to extinction Rate-dependence Visual stimuli Food Multiple schedule Conditioned reinforcers
We would like to thank Jeb Jones, Matthew Locey, Julie Marusich, Steven Meredith, Alana Rojewski, Kathryn Saulsgiver, and Jesse Slappey for their assistance in conducting this research and reviewing an earlier version of the manuscript. This article was used in partial fulfillment for the requirements of the doctoral degree at the University of Florida for the first author, Bethany R. Raiff. This research was supported by US Public Health grant R03DA019467.
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