Disruption of autoshaped responding to a single of brain-stimulation reward by neuroleptic drugs.
Repeated pairing of the onset of a stationary light (CS) that signalled electrical stimulation of brain-stimulation reward sites in the mesencephalon (US) resulted in autoshaped approach behavior to the CS. After acquisition of approach to the CS two groups of rats were injected with either pimozide (0.15, 0.50, or 1.0 mg/kg) or haloperidol (0.05, 0.10, or 0.15 mg/kg) prior to test sessions consisting of 30 CS-US pairings. Both neuroleptic drugs caused a significant dose-related attenuation of the autoshaped CS-approach. A within-session analysis of responding after treatment with the high dose of each drug indicated that most responses occurred in the first 10 trials, a result that appears to rule out a direct effect of the drugs on sensory processes and orientation. The effect of repeated testing with pimozide (1.0 mg/kg) or haloperidol (0.15 mg/kg) was compared to three sessions with CS alone (extinction). Autoshaped CS-approaches declined gradually over the three extinction sessions, in contrast to the immediate and sustained disruption of approaching during the three drug sessions. These data suggest that neuroleptic-induced suppression of autoshaped CS-approach with brain-stimulation reward cannot be attributed solely to a block of reward processes. It is suggested that neuroleptic drugs disrupt neural mechanisms by which signals of impending reward release pre-organized response patterns.
D000818:Animals; D001921:Brain / Q000502:physiology; D003214:Conditioning, Classical / Q000187:drug effects*; D004558:Electric Stimulation; D006220:Haloperidol / Q000494:pharmacology*; D008297:Male; D010775:Photic Stimulation; D010868:Pimozide / Q000494:pharmacology*; D051381:Rats; D011954:Receptors, Dopamine / Q000502:physiology; D012201:Reward
D011954:Receptors, Dopamine; D010868:Pimozide; D006220:Haloperidol