The MacArthur Communicative Development Inventories (CDIs) are a pair of widely used parent-report instruments for assessing communicative skills in infants and toddlers. This report describes short-form versions of the CDIs and their development, summarizes newly available normative data and psychometric properties of the instruments, and discusses research and clinical applications. The infant short form (Level I, for 8- to 18-month-olds) contains an 89-word checklist for vocabulary comprehension and production. The two parallel versions of the toddler short form (Level II, Forms A and B, for 16- to 30-month-olds) each contain a 100-word vocabulary production checklist and a question about word combinations. The forms may also be useful with developmentally delayed children beyond the specified age ranges. Copies of the short forms and the normative tables appear in the appendices.

Naturally occurring impulsive choice has been found to positively predict alcohol consumption in rats. However, the extent to which experimental manipulation of impulsive choice may modify alcohol consumption remains unclear. In the present study, we sought to: (a) train low levels of impulsive choice in rats using early, prolonged exposure to reward delay, and (b) determine the effects of this manipulation on subsequent alcohol consumption. During a prolonged training regimen, three groups of male, adolescent Long-Evans rats (21-22 days old at intake) responded on a single lever for food rewards delivered after either a progressively increasing delay, a fixed delay, or no delay. Post-tests of impulsive choice were conducted, as was an evaluation of alcohol consumption using a limited-access, two-bottle test. Following delay-exposure training, both groups of delay-exposed rats made significantly fewer impulsive choices than did rats in the no-delay group. In addition, fixed-delay rats consumed significantly more alcohol during daily, 30-min sessions than no-delay rats. Possible mechanisms of these effects are discussed, as is the significance of these findings to nonhuman models of addiction.

Delay discounting describes the tendency for organisms to devalue outcomes because they are delayed. Robust, positive correlations exist between excessive delay discounting and many maladaptive behaviors (e.g., substance abuse, obesity). Several studies have demonstrated that delay discounting can be reduced and this may hold promise for improving treatment outcomes. One method of reducing delay discounting provides rats with extended training with delayed reinforcement (i.e., delay-exposure training) and this significantly reduces impulsive choices, relative to rats trained with an equal number of immediate-reinforcement sessions (i.e., immediate-exposure training). To evaluate the stability of this effect, 12 weanling male Wistar rats were randomly assigned to receive either delay-exposure or immediate-exposure training for 120 sessions. Impulsive choice was assessed using an increasing-delay procedure immediately following training and 120 days after completion of the initial assessment. Delay-exposed rats discounted delayed food rewards significantly less than immediate-exposed rats in the initial assessment and the reassessment conducted 120 days later. These results are encouraging as they suggest that the effects of delay-exposure training are robust to the passage of time and intervening experience.

In a prior study (Stein et al., 2013), we reported that rats pre-exposed to delayed rewards made fewer impulsive choices, but consumed more alcohol (12% wt/vol), than rats pre-exposed to immediate rewards. To understand the mechanisms that produced these findings, we again pre-exposed rats to either delayed (17.5 s; n = 32) or immediate (n = 30) rewards. In post-tests, delay-exposed rats made significantly fewer impulsive choices at both 15- and 30-s delays to a larger, later food reward than the immediacy-exposed comparison group. Behavior in an open-field test provided little evidence of differential stress exposure between groups. Further, consumption of either 12% alcohol or isocaloric sucrose in subsequent tests did not differ between groups. Because Stein et al. introduced alcohol concentration gradually (3–12%), we speculate that their group differences in 12% alcohol consumption were not determined by alcohol’s pharmacological effects, but by another variable (e.g., taste) that was preserved as an artifact from lower concentrations. We conclude that pre-exposure to delayed rewards generalizes beyond the pre-exposure delay; however, this same experimental variable does not robustly influence alcohol consumption.

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