The inhibitory potency of SCH 23390 and raclopride on licking for sucrose increases across brief-access tests.

There is extensive pharmacological and microdialysis evidence that central dopamine mechanisms are important for the mediation of the rewarding and reinforcing functions of sweet taste. One aspect of the pharmacological evidence for dopaminergic mediation of sweet reward is unclear. That is the positive interactive effect of ingestive experience and DA antagonist treatment reported by Wise and his colleagues in 1978 [1]. They showed that the inhibitory potency of pimozide increased over repetitive tests of saccharin (0.1%) ingestion. When pimozide was given before 8 daily, 10-minute tests in rats licking [2] or lever pressing [3] for 32% sucrose, however, the inhibitory effect of pimozide did not increase across tests. To reinvestigate the problem, we used a computer-assisted, repetitive, brief-access technique [4, 5] in which 10 male, non-deprived, Sprague Dawley rats licked 0.5M sucrose for 60s in four trials with a 30-second intertrial interval. Thirty minutes before the first trial, each rat received an ip injection of the D1 antagonist SCH 23390, the D2/3 antagonist raclopride, or vehicle. SCH 23390 and raclopride decreased licking significantly, their inhibitory effects increased significantly within and across the 4 trials, and the temporal pattern of their inhibitory effects on latencies, and on cumulative and total licks was different. Thus we confirm an increase of the inhibitory potency of DA antagonists across ingestive tests and show for the first time that the interaction differs between D1 and D2/3 antagonists.