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BACKGROUND This study examined the associations among selective breeding for alcohol preference, intake of sweet solutions, and responding for brain stimulation reward (BSR), a nonoral reinforcer, in alcohol-preferring high-alcohol-drinking (HAD)-1 and nonpreferring low-alcohol-drinking (LAD)-1 rats.METHODS Adult male HAD-1 and LAD-1 rats were trained to lever press for medial forebrain bundle stimulation. Current intensity was varied in separate sessions to generate a rate/intensity function. To further examine BSR responding, the animals responded for stimulation at 100 Hz and at a fixed current intensity on an FR1 schedule. In subsequent sessions, the schedule was increased to FR6 and then to FR12. To examine responding for the sucrose solution, we trained a separate group of HAD-1/LAD-1 rats to bar press for sucrose on an FR1 schedule. Similar to the BSR experiment, in following sessions, the schedule was increased to an FR6 and then to an FR12 schedule.RESULTS No significant differences were observed between the two rat lines across a range of current intensities. As the reinforcement schedule increased, HAD-1 rats exhibited a dramatic decrease in BSR responding, whereas the LAD-1 rats displayed a more protracted reduction. In contrast to BSR, marked elevations in responding were observed for sucrose as the schedule increased. However, in HAD-1 rats, response rates were similar on the FR6 and FR12 schedules, whereas LAD-1 rats showed a reduction in response rates from the FR6 to FR12 schedule. Furthermore, HAD-1 rats exhibited significantly more responses compared with LAD-1 rats across the three reinforcement schedules. An analysis of the response profile for the three reinforcement schedules suggested that few if any postreinforcement pauses were exhibited when the reinforcer was BSR compared with sucrose in both lines.CONCLUSION Medial forebrain bundle BSR is a powerful reinforcer in both HAD-1 and LAD-1 lines. However, BSR responding was not associated with selective breeding for alcohol preference. In contrast, selective breeding for alcohol preference was associated with sucrose consumption, especially as the amount of work increased. The lack of correspondence between BSR and sweet taste rewards in HAD-1 and LAD-1 lines may suggest important differences yet an overlapping brain reward mechanism in the control of motivated behaviors in these selected lines. [ABSTRACT FROM AUTHOR]

Recent studies have implicated the bed nucleus of the stria terminalis (BST) as a potential brain substrate for mediating drug-related behaviors. Neuroanatomical studies have demonstrated that reciprocal projections exist from the BST to the ventral tegmental area (VTA), a dopamine reward substrate proposed to play a role in alcohol abuse. In the present study, we evaluated the role of the D1 and D2 dopamine receptors of the BST in regulating alcohol and sucrose-motivated behaviors. Alcohol-preferring (P) rats were trained under an FR4 operant schedule to self-administer either EtOH (10% v/v) or sucrose (2% w/v). Following training, we evaluated the capacity of a competitive D1 (SCH 23390; 0.5–20.0 μg) and a D2 (eticlopride; 0.5–20.0 μg) dopamine antagonist to selectively reduce EtOH-maintained responding. Naltrexone, (5–30.0 μg), the nonselective opioid antagonist, was used as a reference agent. The results showed that SCH 23390 dose-dependently reduced alcohol-motivated responding. Responding was reduced with the 20.0 μg dose to about 97% of control levels. SCH 23390 also reduced sucrose responding; however, the magnitude of effects was substantially lower with the highest doses (2.5, 20.0 μg) (68–79% of control levels). In contrast, eticlopride failed to significantly alter alcohol responding and reduced sucrose responding only with the 10.0 μg dose. Unlike the dopamine antagonists, all naltrexone doses failed to alter EtOH or sucrose-maintained responding. The results suggest a salient role for the D1, but not the D2 and opioid receptors in selectively modulating EtOH-motivated behaviors in the BST. Synapse 48:45–56, 2003. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]