Background 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. The current study investigated this possibility by assessing three strains of rats previously identified to exhibit heritable differences in ethanol-seeking and consumption. Methods In an adjusting amount delay discounting task, alcohol-preferring P rats who display high levels of both ethanol-seeking and consumption were compared to High Alcohol Drinking (HAD2) rats who only exhibit moderate ethanol-seeking despite high levels of consumption, and Long Evans (LE) rats who display moderate seeking and consumption. Ethanol-seeking and consumption phenotypes were subsequently confirmed in an operant self-administration task with a procedural separation between ethanol-seeking and drinking. Results P rats discounted delayed rewards to a greater extent than both HAD2s and LE who did not show differences in discounting. Moreover, the ethanol-seeking and drinking phenotypes were replicated with P rats displaying greater ethanol-seeking compared to both the HAD2s and LE, and both the HAD2s and P rats consuming more ethanol than LEs. Conclusions 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 since 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.

Background Increased levels of impulsivity are associated with increased illicit drug use and alcoholism. Previous research in our lab has shown that increased levels of delay discounting (a decision-making form of impulsivity) are related to appetitive processes governing alcohol self-administration as opposed to purely consummatory processes. Specifically, the high seeking/high drinking alcohol preferring P rats showed increased delay discounting compared to nonselected Long Evans rats (LE) whereas the high drinking/moderate seeking HAD2 rats did not (Beckwith & Czachowski, 2014). The P rats also displayed a perseverative pattern of behavior such that during operant alcohol self-administration they exhibited greater resistance to extinction. Methods One explanation for the previous findings is that P rats have a deficit in response inhibition. The current study followed up on this possibility by utilizing a countermanding paradigm [stop signal reaction time (SSRT) task] followed by operant self-administration of alcohol across increasing fixed ratio requirements (FR; 1, 2, 5, 10 & 15 responses). In separate animals, 24hr access 2-bottle choice (10% EtOH vs. water) drinking was assessed. Results In the SSRT task, P rats exhibited an increased SSRT compared to both LE and HAD2 rats indicating a decrease in behavioral inhibition in the P rats. Also, P rats showed increased operant self-administration across all FRs and the greatest increase in responding with increasing FR requirements. Conversely, the HAD2 and LE had shorter SSRT, and lower levels of operant alcohol self-administration. However, for 2 bottle choice drinking HAD2s and P rats consumed more EtOH as well as had a greater preference for EtOH compared to LE. Conclusions These data extend previous findings showing the P rats to have increased delay discounting (decision-making impulsivity) and suggest that P rats also have a lack of behavioral inhibition (motor impulsivity). This supports the notion that P rats are a highly impulsive as well as “high seeking” model of alcoholism, and that the HAD2s elevated levels of alcohol consumption are not mediated via appetitive processes or impulsivity.

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