Increased delay discounting tracks with a high ethanol-seeking phenotype and subsequent ethanol seeking but not consumption.

Abstract

Increased levels of delay discounting have been associated with alcoholism and problematic levels of drinking. Attempts to assess the directionality of this relationship by studying individuals with a family history of alcoholism as well as rodent lines selectively bred for high home cage alcohol preference have yielded discordant results. One possible reason for this discordance is that increased levels of delay discounting may only track with specific processes that lead to addiction vulnerability. This study investigated this possibility by assessing 3 strains of rats previously identified to exhibit heritable differences in ethanol (EtOH) seeking and consumption. In an adjusting amount delay discounting task, alcohol-preferring (P) rats who display high levels of both EtOH seeking and consumption were compared to high alcohol-drinking (HAD2) rats who only exhibit moderate EtOH seeking despite high levels of consumption, and Long Evans (LE) rats who display moderate seeking and consumption. EtOH-seeking and consumption phenotypes were subsequently confirmed in an operant self-administration task with a procedural separation between EtOH seeking and drinking. P rats discounted delayed rewards to a greater extent than both HAD2s and LE who did not show differences in discounting. Moreover, the EtOH-seeking and drinking phenotypes were replicated with P rats displaying greater EtOH seeking compared to both the HAD2s and LE, and both the HAD2s and P rats consuming more EtOH than LEs. Only the high-seeking strain, the P rats, exhibited increased levels of delay discounting. This suggests that this measure of behavioral under-control is specifically associated with alcohol-related appetitive, but not consummatory, processes as the moderate seeking/high drinking line did not show increased levels of impulsivity. This finding supports the hypothesis that delay discounting is specifically associated with only certain processes which are sufficient but not necessary to confer addiction vulnerability and therefore also supports increased levels of delay discounting as a predisposing risk factor for alcoholism.