Dissecting drug effects in preclinical models of impulsive choice: emphasis on glutamatergic compounds

Impulsive choice is often measured with delay discounting paradigms. Because there are multiple discounting procedures, as well as different statistical analyses that can be applied to data generated from these paradigms, there are some inconsistencies in the literature regarding drug effects on impulsive choice.

The goal of the current paper is to review the methodological and analytic approaches used to measure discounting and to discuss how these differences can account for differential drug effects observed across studies.

Because some procedures/analyses use a single data point as the dependent variable, changes in this value following pharmacological treatment may be interpreted as alterations in sensitivity to delayed reinforcement, but when other procedures/analyses are used, no changes in behavior are observed. Even when multiple data points are included, some studies show that the statistical analysis (e.g., ANOVA on raw proportion of responses vs. using hyperbolic/exponential functions) can lead to different interpretations. Finally, procedural differences (e.g., delay presentation order, signaling the delay to reinforcement, etc.) in the same discounting paradigm can alter how drugs affect sensitivity to delayed reinforcement.

Future studies should utilize paradigms that allow one to observe alterations in responding at each delay (e.g., concurrent-chains schedules). Concerning statistical analyses, using parameter estimates derived from nonlinear functions or incorporating the generalized matching law can allow one to determine if drugs affect sensitivity to delayed reinforcement or impair discrimination of the large and small magnitude reinforcers. Using these approaches can help further our understanding of the neurochemical underpinnings of delay discounting.