BROMOCRIPTINE ENHANCEMENT OF RESPONDING FOR CONDITIONED REWARD DEPENDS ON INTACT D-1 RECEPTOR FUNCTION

It has been suggested that reward-related learning may require intact functioning at the dopamine D-1 receptor. The present experiment teste d this hypothesis by challenging the reward-enhancing effects of the D -2 agonist, bromocriptine, with a D-1 antagonist, SCH 23390. For compa rison, the effects of the D-2 antagonist, pimozide, were also evaluate d. Male rats (n = 240) were pre-exposed to a chamber with two levers, one producing a 3-s lights-off stimulus and the other a 3-s tone stimu lus. Four conditioning sessions followed, during which levers were abs ent and presentations of the lights-off stimulus were paired with food . Testing consisted of comparing presses on each lever after condition ing to before conditioning for each rat. Control groups showed a signi ficantly greater increase in responding for lights-off than tone, indi cating that the lights-off stimulus had become a conditioned reward. R esults showed that bromocriptine (0.25-10.0 mg/kg, IF, 60 min before t est session) enhanced responding at doses of 2.5 and 5.0 mg/kg signifi cantly more on the conditioned reward lever than on the other lever. T he lowest dose of SCH 23390 (1.0 mu g/kg, SC, 2 h before testing) elim inated the bromocriptine-produced enhancement at 2.5 mg/kg and a signi ficant enhancement was seen at 10.0 mg/kg. The higher doses of SCH 233 90 (5.0 and 10.0 mu g/kg) eliminated the bromocriptine effect and the conditioned reward effect itself, respectively. The low dose of pimozi de (0.1 mg/kg, IF, 4 h before test session) eliminated the bromocripti ne-produced enhancement at 2.5 and 5.0 mg/kg and a significant enhance ment was now seen at 10.0 mg/kg; the higher dose (0.2 mg/kg) appeared to block the conditioned reward effect itself. These results suggest t hat both SCH 23390 and pimozide interfered with the reward-enhancing e ffects of bromocriptine. Thus, the present results suggest that reward -related learning can be enhanced through D-2 receptor stimulation wit h bromocriptine and that this effect appears to depend on intact D-1 r eceptor function.