Reward and the serotonergic system

Kranz, Georg S.; Kasper, Siegfried; Lanzenberger, Rupert

doi:10.1016/j.neuroscience.2010.01.036

Cited by 220 publications

(164 citation statements)

References 108 publications

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“…Treatment with an SSRI enhanced the negative coupling between the NAcc and the key structure of the serotonergic system, and integrates well with previous ideas on a link between SSRI intake and altered processing of primary rewards (Kranz et al, 2010;Boureau and Dayan, 2011).…”

Section: Discussionsupporting

confidence: 83%

“…Sexual dysfunction, including reduced drive and desire, is a common phenomenon accompanying SSRI intake (Clayton et al, 2002;Serretti and Chiesa, 2009), pointing toward impaired processing of primary rewards. Diminished responsiveness to motivational stimuli under SSRIs has been related to the inhibition of dopaminergic reward circuits by serotonin (Kranz et al, 2010) and is in line with a proposed opponency of dopaminergic and serotonergic effects (Boureau and Dayan, 2011). However, mechanisms remain unclear.…”

Section: Introductionmentioning

confidence: 90%

“…Modulation of the dopaminergic reward system by serotonin is increasingly attracting attention in systems neuroscience (Seo et al, 2008;Kranz et al, 2010;Hayes and Greenshaw, 2011). A prevalent psychopharmacological example for such an interaction is the reward system's downregulation, which has been suggested to account for unsatisfactory effects of antidepressant serotonin reuptake inhibitors (SSRIs).…”

Section: Introductionmentioning

confidence: 99%

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Modulation of Frontostriatal Interaction Aligns with Reduced Primary Reward Processing under Serotonergic Drugs

Abler¹,

Grön²,

Hartmann³

et al. 2012

J. Neurosci.

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Recently, functional interactions between anteroventral prefrontal cortex and nucleus accumbens (NAcc) have been shown to relate to behavior counteracting reward-desiring (Diekhof and Gruber, 2010). Downregulation of the reward system by serotonin has also been suggested as the mode of action accounting for unsatisfactory effects of serotonin reuptake inhibitors (SSRIs) such as insufficient alleviation or even increase of anhedonia, and loss of interest. However, understanding of the in vivo mechanisms of SSRI-related alteration of the human reward system is still incomplete. Using functional magnetic resonance imaging (fMRI) within a double-blind cross-over within-subjects study design and administering the SSRI paroxetine, the dopamine/norepinephrine reuptake inhibitor bupropione, and placebo for 7 d each, we investigated a group of 18 healthy male subjects. Under paroxetine, subjects showed significantly decreased activation of the bilateral NAcc during processing of primary rewards (erotic videos), but not under bupropion. Similar to the previous study, analysis of psychophysiological interactions revealed that this downregulation relied on negative interactions between left and right NAcc fMRI signals and the bilateral anteroventral prefrontal cortex that now were significantly enhanced under paroxetine and reduced under bupropion. Individual drug-dependent modulations of interacting brain regions were significantly associated with individual expressions of impulsivity as a personality trait. Our results corroborate and extend previous insights on interregional crosstalk from secondary to primary rewards and demonstrate parallels between active inhibitory control of and serotonergic effects on the dopaminergic reward system's activity.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Modulation of Frontostriatal Interaction Aligns with Reduced Primary Reward Processing under Serotonergic Drugs

Abler¹,

Grön²,

Hartmann³

et al. 2012

J. Neurosci.

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“…SSRI-dependent modulations of activity in midbrain and ventral striatum align with recent evidence indicating that the functioning of these brain regions is tuned by serotonin (Kranz et al, 2010). The positive activation of these regions upon erotic stimulation in the sense of a primary reward under placebo adds to the accepted interpretation of these brain regions as part of the dopaminergic reward system (Kranz et al, 2010).…”

Section: Ssri-related Alteration Of Midbrain and Ventral Striatum Actsupporting

confidence: 69%

“…The positive activation of these regions upon erotic stimulation in the sense of a primary reward under placebo adds to the accepted interpretation of these brain regions as part of the dopaminergic reward system (Kranz et al, 2010). Despite the inconsistencies concerning the general role of serotonin in reward processing with reports on reward-increasing and reward-decreasing effects of serotonin, the latter results seem more prevalent.…”

Section: Ssri-related Alteration Of Midbrain and Ventral Striatum Actmentioning

confidence: 99%

Neural Correlates of Antidepressant-Related Sexual Dysfunction: A Placebo-Controlled fMRI Study on Healthy Males Under Subchronic Paroxetine and Bupropion

Abler

Seeringer

Hartmann

et al. 2011

Neuropsychopharmacol

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Sexual dysfunction is a common side effect of selective serotonin reuptake inhibitors (SSRIs) like paroxetine in the treatment of depression, imposing a considerable risk on medication adherence and hence therapeutic success. Bupropion, a norepinephrine and dopamine reuptake inhibitor, is recommended as an alternative treatment without adverse effects concerning sexual arousal and libido. We investigated the neural bases of paroxetine-related subjective sexual dysfunction when compared with bupropion and placebo. We scanned 18 healthy, heterosexual males in a randomized, double-blind, within-subject design while watching video clips of erotic and nonerotic content under steady-state conditions after taking 20 mg of paroxetine, 150 mg of bupropion, and placebo for 7 days each. Under paroxetine, ratings of subjective sexual dysfunction increased compared with placebo or bupropion. Activation along the anterior cingulate cortex (ACC), including subgenual, pregenual, and midcingulate cortices, in the ventral striatum and midbrain was decreased when compared with placebo. In contrast, bupropion let subjective ratings and ACC activations unchanged and increased activity of brain regions including posterior midcingulate cortex, mediodorsal thalamus, and extended amygdala relative to placebo and paroxetine. Brain regions that have been related to the processing of motivational (ventral striatum), emotional, and autonomic components of erotic stimulation (anterior cingulate) in previous studies showed reduced responsiveness under paroxetine in our study. Drug effects on these regions may be part of the mechanism underlying SSRI-related sexual dysfunction. Increased activation under bupropion may point to an opposite effect that may relate to the lack of impaired sexual functioning.

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The Intersection between Neurobiological and Psychological Theories of Substance Use Disorders

Baskin‐Sommers¹,

Hearon²

2015

The Handbook of Drugs and Society

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Reward and the serotonergic system

Cited by 220 publications

References 108 publications

Modulation of Frontostriatal Interaction Aligns with Reduced Primary Reward Processing under Serotonergic Drugs

Modulation of Frontostriatal Interaction Aligns with Reduced Primary Reward Processing under Serotonergic Drugs

Neural Correlates of Antidepressant-Related Sexual Dysfunction: A Placebo-Controlled fMRI Study on Healthy Males Under Subchronic Paroxetine and Bupropion

The Intersection between Neurobiological and Psychological Theories of Substance Use Disorders

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