Serotonin-Dopamine Interactions in the Control of Conditioned Reinforcement and Motor Behavior

Sasaki‐Adams, Deanna; Kelley, Ann E.

doi:10.1016/s0893-133x(01)00240-8

Cited by 80 publications

(52 citation statements)

References 74 publications

(96 reference statements)

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“…The latter finding suggests that serotonin affects the way that reward-associated signals influence behaviour; consistent with reports that fluoxetine potentiates the control of ongoing responding by available conditioned reinforcers (Sasaki-Adams and Kelley, 2001;Fletcher et al, 1999). In this context, it is important to note that the results of the present study do not, in themselves, show that tryptophan depletion reduces sensitivity to reward per se rather the data indicate that the TÀ volunteers did not discriminate as effectively as the T+ volunteers between differences in the magnitude of rewards associated with different choices.…”

Section: Discussionsupporting

confidence: 89%

“…Evidence of a role for serotonin in reward processing includes recent demonstrations that the behavioural and reinforcing effects of cocaine in rats are potentiated by treatment with selective serotonin-reuptake blockers (SSRIs) (Cunningham and Callahan, 1991;Kleven and Koek, 1998;Sasaki-Adams and Kelley, 2001), and that brain self-stimulation thresholds can be dose-dependently altered with SSRI treatment (Harrison and Markou, 2001a, b). Also relevant are serotonin's acknowledged involvement in clinical depression (eg Schildkraut, 1965) and the more general observation that SSRI treatment is relatively effective in the treatment of clinical depressive illness, while the temporary reduction of central serotonin function in vulnerable individuals through rapid dietary tryptophan depletion has been shown to reinstate depressive symptoms and flat affect (Moore et al, 2000;Smith et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Tryptophan Depletion Alters the Decision-Making of Healthy Volunteers through Altered Processing of Reward Cues

Rogers

Tunbridge

Bhagwagar

et al. 2002

Neuropsychopharmacol

253

231

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While accumulating evidence suggests that effective real-life decision-making depends upon the functioning of the orbitofrontal cortex, much less is known about the involvement of the monoamine neurotransmitter systems and, in particular, serotonin. In the present study, we explored the impact of depleting the serotonin precursor, tryptophan, on human decision-making. Eighteen healthy volunteers consumed an amino-acid drink containing tryptophan and 18 healthy volunteers consumed an amino-acid drink without tryptophan, before choosing between simultaneously presented gambles, differing in the magnitude of expected gains (ie reward), the magnitude of expected losses (ie punishment), and the probabilities with which these outcomes were delivered. Volunteers also chose between gambles probing identified non-nomative biases in human decision-making, namely, risk-aversion when choosing between gains and riskseeking when choosing between losses. Tryptophan-depleted volunteers showed reduced discrimination between magnitudes of expected gains associated with different choices. There was little evidence that tryptophan depletion was associated with altered discrimination between the magnitudes of expected losses, or altered discrimination between the relative probabilities with which these positive or negative outcomes were delivered. Risk-averse and risk-seeking biases were also unchanged. These results suggest that serotonin mediates decision-making in healthy volunteers by modulating the processing of reward cues, perhaps represented within the orbitofrontal cortex. It is possible that such a change in the cognition mediating human choice is one mechanism associated with the onset and maintenance of anhedonia and lowered mood in psychiatric illness.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Tryptophan Depletion Alters the Decision-Making of Healthy Volunteers through Altered Processing of Reward Cues

Rogers

Tunbridge

Bhagwagar

et al. 2002

Neuropsychopharmacol

253

231

View full text Add to dashboard Cite

show abstract

“…Serotonin (5-HT) has been extensively implicated in depressed mood and is well known to affect the motivational properties of stimuli predictive of rewards (Fletcher et al, 1999;Sasaki-Adams and Kelley, 2001;Deakin, 1983;Wilkinson et al, 1995;Graeff et al, 1986), probably through interaction with the mesolimbic dopamine (DA) system (Robbins et al, 1989;Robbins and Everitt, 2002). Treatment with selective serotonin reuptake inhibitors (SSRIs) dose dependently decreases brain self-stimulation thresholds (Harrison and Markou, 2001), while the reinforcing effects of cocaine, cocaine-associated stimuli, and other stimuli predictive of rewards are potentiated by SSRI treatment and, conversely, attenuated by central 5-HT depletion (Aronson et al, 1995;Sasaki-Adams and Kelley, 2001;Redgrave and Horrell, 1976).…”

Section: Introductionmentioning

confidence: 99%

“…Treatment with selective serotonin reuptake inhibitors (SSRIs) dose dependently decreases brain self-stimulation thresholds (Harrison and Markou, 2001), while the reinforcing effects of cocaine, cocaine-associated stimuli, and other stimuli predictive of rewards are potentiated by SSRI treatment and, conversely, attenuated by central 5-HT depletion (Aronson et al, 1995;Sasaki-Adams and Kelley, 2001;Redgrave and Horrell, 1976).…”

Section: Introductionmentioning

confidence: 99%

Tryptophan Depletion Disrupts the Motivational Guidance of Goal-Directed Behavior as a Function of Trait Impulsivity

Cools

Blackwell

Clark

et al. 2005

Neuropsychopharmacol

143

145

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Serotonin (5-HT) is well known to affect the motivational properties of stimuli predictive of rewards as well as the inhibitory control of behavior. Here, central 5-HT depletion was induced by the acute tryptophan (TRP) depletion (ATD) procedure in young healthy volunteers to examine the role of 5-HT in motivated action and prepotent response inhibition. A novel reaction-time task, tailored to individual differences in general cognitive speed, was employed to measure the guidance of behavior by motivationally relevant signals predictive of reinforcement likelihood, while the stop-signal reaction-time task was used to measure response inhibition. Following the TRP-balancing control drink, cues predictive of high-reinforcement certainty induced faster, but less accurate responses compared with cues predictive of lower reinforcement certainty. Depletion of central 5-HT modulated this coupling between motivation and action by slowing responses and increasing accuracy as a function of incentive certainty. These effects of ATD on motivated action correlated highly with individual differences in the personality trait of Nonplanning Impulsiveness (Barratt Impulsivity Scale (BIS-11)), so that strongest effects on motivated action were observed in high-impulsive individuals. By contrast, ATD left unaltered the ability to inhibit prepotent responses. Our findings may have implications for a variety of neuropsychiatric disorders including impulsive aggressive disorders and depression.

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“…Accumbal 5-HT levels were increased in all treatments relative to undisturbed controls. These rapid increases in NAc 5-HT levels following brief social threat or environmental disturbance may either facilitate NAc DA-mediated motivational behaviors [47,48], or enhance survival by reducing expression of inappropriate behavior in aversive contexts [49,50].…”

Section: Effects Of Social Threat On Limbic Monoaminesmentioning

confidence: 99%

Rapid neuroendocrine responses evoked at the onset of social challenge

Watt

Forster

Korzan

et al. 2007

Physiology & Behavior

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At the onset of agonistic social challenge, individuals must assess the degree of threat the opponent represents in order to react appropriately. We aimed to characterize the neuroendocrine changes accompanying this period of initial social assessment using the lizard Anolis carolinensis. Conveyance of aggressive intent by male A. carolinensis is facilitated by rapid post-orbital skin darkening (eyespot), whereas eyespot presence inhibits opponent aggression. By manipulating this visual signal, we also investigated whether differing neuroendocrine changes were evoked by initial presentation of varying levels of social threat. Subjects were painted postorbitally either with black paint (high threat level), green paint (low threat level) or water (controls). Painted animals were presented with a mirror and sampled immediately upon exhibiting aggressive intent towards the reflected simulated opponent, but before producing behaviors such as motor pattern-based displays. Control animals (blank surface presented) were sampled at times derived from averaging response times of painted subjects. Brains and plasma were analyzed for monoamine activity and catecholamine levels using electrochemical HPLC. Social threat evoked increases in plasma catecholamine levels indistinguishable from those caused by brief environmental disturbance. However, brief social challenge caused distinct rapid increases in amygdala and nucleus accumbens (NAc) dopamine and serotonin levels. Amygdalar changes were associated with general social threat presence, but NAc monoamines were affected by both threat level and subject motivation to engage in confrontation. This suggests that specific rapid activity changes in key forebrain limbic nuclei differ according to the degree of social threat perceived at the start of the interaction.

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Serotonin-Dopamine Interactions in the Control of Conditioned Reinforcement and Motor Behavior

Cited by 80 publications

References 74 publications

Tryptophan Depletion Alters the Decision-Making of Healthy Volunteers through Altered Processing of Reward Cues

Tryptophan Depletion Alters the Decision-Making of Healthy Volunteers through Altered Processing of Reward Cues

Tryptophan Depletion Disrupts the Motivational Guidance of Goal-Directed Behavior as a Function of Trait Impulsivity

Rapid neuroendocrine responses evoked at the onset of social challenge

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