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  • 1
    ISSN: 1432-2072
    Keywords: Extinction ; Pimozide ; SCH 23390 ; Metoclopramide ; Reward ; Dopamine ; D1 receptors ; D2 receptors ; Variable interval schedule ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The similarity in the pattern of responding produced by extinction and dopamine (DA) receptor blockers has led to the suggestion that DA neurons may participate in the usual effects of reward on behaviour. The purpose of the present study was to evaluate the effect of receptor-subtype specific DA antagonists on food-rewarded operant responding. Rats were trained to lever press for food on a variable interval 30-s schedule. They then received one of the following treatments prior to testing on the next 5 days: saline, nonreinforcement, the DA receptor blocker pimozide (0.5 or 1.0 mg/kg), the D1 receptor blocker SCH 23390 (0.01, 0.05, 0.1 mg/kg), and the D2 receptor blocker metoclopramide (1.0, 5.0, 10.0 mg/kg). Nonreinforcement resulted in both intra- and intersession declines in responding. The drugs produced dose-dependent decreases in overall responding. Additionally, both doses of pimozide and the higher doses of SCH 23390 and metoclopramide altered intrasession patterns of responding when compared to saline, with their greatest effect being in the latter portion of the session. Intersession declines were seen with the highest doses of SCH 23390 and metoclopramide and control studies showed that these declines could not be attributed to a buildup of the drug with repeated dosing. It was concluded that both D1 and D2 receptors participate in the control of behaviour by reward.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 118 (1995), S. 437-443 
    ISSN: 1432-2072
    Keywords: Bromocriptine ; Conditioned reward ; D1 receptors ; D2 receptors ; Dopamine ; Reinforcement ; Reward ; SCH 23390
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been suggested that reward-related learning may require intact functioning at the dopamine D1 receptor. The present experiment tested this hypothesis by challenging the reward-enhancing effects of the D2 agonist, bromocriptine, with a D1 antagonist, SCH 23390. For comparison, the effects of the D2 antagonist, pimozide, were also evaluated. 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 stimulus. Four conditioning sessions followed, during which levers were absent and presentations of the lights-off stimulus were paired with food. Testing consisted of comparing presses on each lever after conditioning to before conditioning for each rat. Control groups showed a significantly greater increase in responding for lights-off than tone, indicating that the lights-off stimulus had become a conditioned reward. Results showed that bromocriptine (0.25–10.0 mg/kg, IP, 60 min before test session) enhanced responding at doses of 2.5 and 5.0 mg/kg significantly more on the conditioned reward lever than on the other lever. The lowest dose of SCH 23390 (1.0 µg/kg, SC, 2 h before testing) eliminated the bromocriptine-produced enhancement at 2.5 mg/kg and a significant enhancement was seen at 10.0 mg/kg. The higher doses of SCH 23390 (5.0 and 10.0 µg/kg) eliminated the bromocriptine effect and the conditioned reward effect itself, respectively. The low dose of pimozide (0.1 mg/kg, IP, 4 h before test session) eliminated the bromocriptine-produced enhancement at 2.5 and 5.0 mg/kg and a significant enhancement 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 that both SCH 23390 and pimozide interfered with the reward-enhancing effects of bromocriptine. Thus, the present results suggest that reward-related learning can be enhanced through D2 receptor stimulation with bromocriptine and that this effect appears to depend on intact D1 receptor function.
    Type of Medium: Electronic Resource
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