How do genotype, stimulus conditions, and acute dopaminergic administration interact to influence the temporal allocation of credit?

Abstract

The importance of delay discounting to many socially important behavioral problems has led to investigations of the genetic, biochemical, and environmental mechanisms responsible for variations in the form of the discount function, but the extant experimental research in these areas has yielded disparate results. The present study examined potential Gene X Drug X Environment interactions in delay discounting by examining d-amphetamine’s effects on delay discounting in two mouse strains using a novel procedure. BALB/c and C57BL/6 mice responded on a six-component concurrent-chained schedule in which the order of terminal-link delays preceding a larger-reinforcer was randomized across components. Across conditions, components were presented as mixed or multiple schedules and effects of a dose-range of d-amphetamine were determined. Dose-effects on generalized matching sensitivity to reinforcer magnitude and delay were characterized by multi-model inference. For BALB/cs, there were no effects of schedule on model parameters under control conditions, however, d-amphetamine dose-dependently decreased delay sensitivity and this effect was greater under the mixed schedule. For C57BL/6s, control estimates of sensitivity to reinforcement were higher under the multiple schedule and d-amphetamine dose-dependently decreased sensitivity to reinforcement under the multiple and increased sensitivity to reinforcement under the mixed schedule. These results suggest a genotype X environment interaction describing d-amphetamine’s effects on delay discounting. Differences in the baseline form of the discount function were generated by a genotype X signaling condition interaction and the effects of d-amphetamine were baseline-dependent.