Conclusions
Results from experiment 1 suggest that when LEW and F344 are pair housed, there are no strain differences in delay discounting in response to nicotine. Results from experiment 2 suggest that attenuation of nicotine's effects on delay discounting may not be specific to nAChR antagonism.
Methods
Male LEW and F344 were trained to choose between one food pellet delivered immediately and three food pellets delivered after an increasing delay. During experiment 1, saline and nicotine (0.1-1.0 mg/kg) were tested acutely. During experiment 2, mecamylamine (0.25-1.0 mg/kg) or a nonselective mAChR antagonist, scopolamine (0.01-0.056 mg/kg), was administered prior to nicotine administration.
Objective
During experiment 1, we evaluated dose-dependent effects of nicotine on delay discounting of pair-housed Lewis (LEW) and Fischer 344 (F344) rats. During experiment 2, we examined the sensitivity of nicotine's effects on delay discounting to pharmacological antagonism of nAChRs or muscarinic AChRs (mAChRs). Materials and
Results
Nicotine dose dependently reduced delay discounting for both rat strains, and no strain differences were observed (ΔAUC = + 107% for 1.0 mg/kg and + 69.6% for 0.3 mg/kg relative to saline). At some doses, pretreatment with mecamylamine (range ΔAUC = - 27.6 to - 7.3%) or scopolamine (range ΔAUC = - 0.74 to - 51.6%) significantly attenuated the nicotine-induced reduction in some measures of delay discounting for both strains. Conclusions: Results from experiment 1 suggest that when LEW and F344 are pair housed, there are no strain differences in delay discounting in response to nicotine. Results from experiment 2 suggest that attenuation of nicotine's effects on delay discounting may not be specific to nAChR antagonism.