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.