Effects of dopamine receptor blockade on alimentary behaviors: Home cage food consumption, magazine training, operant acquisition, and performance

Tombaugh, Tom N.; Tombaugh, Jo W.; Anisman, Hymie

doi:10.1007/bf00428309

Cited by 123 publications

(28 citation statements)

References 10 publications

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“…Consistent with previous reports from operant procedures (e.g., Tombaugh et al, 1979; Wise and Schwartz, 1981) the administration of dopamine antagonists during training severely retarded the rate of responding in both sensitized and non-sensitized animals. It is important to note that, despite these reduced rates, all animals earned the same number of reinforcers during training as session length was limited by the number of reinforcers earned and not time (Adams, 1982).…”

Section: Discussionsupporting

confidence: 90%

Accelerated habit formation following amphetamine exposure is reversed by D1, but enhanced by D2, receptor antagonists

Nelson¹,

Killcross²

2013

Front. Neurosci.

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Repeated exposure to the psychostimulant amphetamine has been shown to disrupt goal-directed instrumental actions and promote the early and abnormal development of goal-insensitive habitual responding (Nelson and Killcross, 2006). To investigate the neuropharmacological specificity of this effect as well as restore goal-directed responding in animals with pre-training amphetamine exposure, animals were treated with the non-selective dopamine antagonist α-flupenthixol, the selective D1 antagonist SCH 23390 or the selective D2 antagonist eticlopride, prior to instrumental training (three sessions). Subsequently, the reinforcer was paired with LiCL-induced gastric-malaise and animals were given a test of goal-sensitivity both in extinction and reacquisition. The effect of these dopaminergic antagonists on the sensitivity of lever press performance to outcome devaluation was assessed in animals with pre-training exposure to amphetamine (Experiments 1A–C) or in non-sensitized animals (Experiment 2). Both α-flupenthixol and SCH23390 reversed accelerated habit formation following amphetamine sensitization. However, eticlopride appeared to enhance this effect and render instrumental performance compulsive as these animals were unable to inhibit responding both in extinction and reacquisition, even though a consumption test confirmed they had acquired an aversion to the reinforcer. These findings demonstrate that amphetamine induced-disruption of goal-directed behavior is mediated by activity at distinct dopamine receptor subtypes and may represent a putative model of the neurochemical processes involved in the loss of voluntary control over behavior.

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Section: Discussionsupporting

confidence: 90%

Accelerated habit formation following amphetamine exposure is reversed by D1, but enhanced by D2, receptor antagonists

Nelson¹,

Killcross²

2013

Front. Neurosci.

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“…The evidence is a decrease in the asymptotic response rate and further increases in the rate of reinforcement necessary for a one-half asymptotic response rate. Wise (1982) and others (e.g., Gallistel and Karras 1984) concluded that neuroleptics reduced reinforcement efficacy, whereas Tombaugh et al (1979) and others (e.g., Ettenberg et al 1981) concluded that neuroleptics affect motor performance. The matching law approach provides a quantitative index for each interpretation, and according to these quantitative criteria both interpretations are to some extent correct.…”

Section: Discussionmentioning

confidence: 99%

Chlorpromazine and pimozide alter reinforcement efficacy and motor performance

1986

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This study evaluated the effects of chlorpromazine and pimozide on reinforced responding. In each session, rats were exposed to a series of five variable-interval reinforcement schedules. The response requirement was a lever press, the reward was a small portion of water, and the reinforcement rate varied from about 20 to 660 reinforcers per hour. Response rate was a negatively accelerated function of reinforcement rate, and the relationship between the two variables was described by the equation for a rectangular hyperbola (the matching law). One parameter of the hyperbola is equivalent to the asymptotic response rate and the other parameter is equivalent to the rate of reinforcement that maintains a one-half asymptotic response rate. Chlorpromazine (0.75-3.0 mg/kg) and pimozide (0.1-0.4 mg/kg) dose-dependently decreased response rates. At low doses, the response rate decreases were, for the most part, restricted to the low reinforcement rate schedules. In contrast, the highest dose tested decreased response rates at both low and high reinforcement rates. The patterns of response rate decreases resulted in dose-dependent changes in the parameters of the matching law equation. The shifts in the matching law parameters were discussed in terms of the motoric and motivational interpretations of neuroleptic-induced response rate changes.

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“…Thus the habit-forming effect of food is severely attenuated by dopamine blockade. These findings have not been challenged but have rather been replicated by critics of what has come to be labeled the anhedonia hypothesis (Tombaugh et al , 1979; Mason et al , 1980), who have argued that under their conditions neuroleptics cause performance deficits above and beyond clear deficits in reinforcement. Given the fact that neuroleptics block all dopamine systems, some of which are thought to be involved in motor function, this was not surprising or contested (Wise, 1985).…”

Section: The Hypothesesmentioning

confidence: 99%

Dopamine and reward: The anhedonia hypothesis 30 years on

2008

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The anhedonia hypothesis – that brain dopamine plays a critical role in the subjective pleasure associated with positive rewards – was intended to draw the attention of psychiatrists to the growing evidence that dopamine plays a critical role in the objective reinforcement and incentive motivation associated with food and water, brain stimulation reward, and psychomotor stimulant and opiate reward. The hypothesis called to attention the apparent paradox that neuroleptics, drugs used to treat a condition involving anhedonia (schizophrenia), attenuated in laboratory animals the positive reinforcement that we normally associate with pleasure. The hypothesis held only brief interest for psychiatrists, who pointed out that the animal studies reflected acute actions of neuroleptics whereas the treatment of schizophrenia appears to result from neuroadaptations to chronic neuroleptic administration, and that it is the positive symptoms of schizophrenia that neuroleptics alleviate, rather than the negative symptoms that include anhedonia. Perhaps for these reasons, the hypothesis has had minimal impact in the psychiatric literature. Despite its limited heuristic value for the understanding of schizophrenia, however, the anhedonia hypothesis has had major impact on biological theories of reinforcement, motivation, and addiction. Brain dopamine plays a very important role in reinforcement of response habits, conditioned preferences, and synaptic plasticity in cellular models of learning and memory. The notion that dopamine plays a dominant role in reinforcement is fundamental to the psychomotor stimulant theory of addiction, to most neuroadaptation theories of addiction, and to current theories of conditioned reinforcement and reward prediction. Properly understood, it is also fundamental to recent theories of incentive motivation.

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Effects of dopamine receptor blockade on alimentary behaviors: Home cage food consumption, magazine training, operant acquisition, and performance

Cited by 123 publications

References 10 publications

Accelerated habit formation following amphetamine exposure is reversed by D1, but enhanced by D2, receptor antagonists

Accelerated habit formation following amphetamine exposure is reversed by D1, but enhanced by D2, receptor antagonists

Chlorpromazine and pimozide alter reinforcement efficacy and motor performance

Dopamine and reward: The anhedonia hypothesis 30 years on

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