In response to the accident at the Fukushima Daiichi nuclear power station in Japan, the U.S. Nuclear Regulatory Commission (NRC) and Department of Energy agreed to jointly sponsor an accident reconstruction study as a means of assessing severe accident modeling capability of the MELCOR code. MELCOR is the state-of-the-art system-level severe accident analysis code used by the NRC to provide information for its decision-making process in this area. The objectives of the project were: (1) collect, verify, and document data on the accidents by developing an information portal system; (2) reconstruct the accident progressions using computer models and accident data; and (3) validate the MELCOR code and the Fukushima models, and suggest potential future data needs. Idaho National Laboratory (INL) developed an information portal for the Fukushima Daiichi accident information. Sandia National Laboratories (SNL) developed MELCOR 2.1 models of the Fukushima Daiichi Units 1, 2, and 3 reactors and the Unit 4 spent fuel pool. Oak Ridge National Laboratory (ORNL) developed a MELCOR 1.8.5 model of the Unit 3 reactor and a TRACE model of the Unit 4 spent fuel pool. The good correlation of the results from the SNL models with the data from the plants and with the ORNL model results provides additional confidence in the MELCOR code. The modeling effort has also provided insights into future data needs for both model development and validation.
RATIONALE
Nicotine discontinuation produces behaviors in rats that are congruent with anhedonia, and these symptoms may be related to the devaluation of non-nicotine reinforcers.
OBJECTIVE
Four separate experiments were performed to explore the parameters surrounding nicotine-induced reinforcer devaluation.
METHODS
In Experiments 1 and 2, nicotine (0.1 or 0.3 mg/kg) or 0.3 mg/kg nicotine plus 1.0 mg/kg mecamylamine was delivered to rats prior to progressive ratio (PR) schedule sessions in which sucrose was used as a reinforcer. In order to (a) evaluate reinforcer enhancement by nicotine, and (b) reinforcer devaluation in the absence of nicotine, all rats experienced two PR schedule sessions per day for 10 days. Experiment 3 involved nicotine (0.3 mg/kg) and a visual stimulus in place of sucrose reinforcement. In Experiment 4, rats received nicotine (0.3 mg/kg) either before or after a single PR-schedule session for 10 days.
RESULTS
Experiments 1 and 2 demonstrate that reinforcer devaluation is related to the occupation of nicotinic-acetylcholine receptors. Results from Experiment 3 provide some evidence that devaluation occurs with either sucrose or visual-stimulus reinforcement. Experiment 4 demonstrates that a necessary condition for reinforcer devaluation to occur is the concurrent exposure to the reinforcer and nicotine.
CONCLUSIONS
Reinforcer devaluation in rats emerges rapidly in a progressive, orderly fashion that coincides with accumulated exposure to nicotine. These results suggest that reinforcer devaluation may be a feature of nicotine that contributes to the abuse liability of tobacco products.
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