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Aberrant reward dynamics in trait anticipatory anhedonia.

ABSTRACT: As a cardinal feature of several psychiatric disorders, anhedonia includes a consummatory component (deficits in hedonic response to rewards) and an anticipatory component (a reduced motivation to pursue them). Although being conceptualized as impairments of reward system, the neural characterization of reward processing in anhedonia is hampered by the enormous heterogeneity in the reward phase ('wanting' vs 'liking') and comorbidity (inherent to disease states). The current event-related potential (ERP) study examined the reward dynamics of anticipatory anhedonia in a non-clinical sample. Anticipatory and consummatory ERP components were assessed with a monetary incentive delay task in a high anticipatory anhedonia (HAA) group and a low anticipatory anhedonia (LAA) group. HAA vs LAA group showed a diminished reward-related speeding during behavioral performance and reported overall reduced positive affect during anticipation and receipt of outcomes. Importantly, neural dynamics underlying reward processing were negatively associated with anticipatory anhedonia across the anticipatory phase indexed by the contingent negative variation and the consummatory phase indexed by the feedback P3. Our results suggest that anticipatory anhedonia in non-clinical individuals is linked to a poor modulation during both anticipatory and consummatory phases of reward processing.

SUBMITTER: Zhou S

PROVIDER: S-EPMC6847339 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Aberrant reward dynamics in trait anticipatory anhedonia.

Zhou Shiyu S Nie Lu L Wang Zhao Z Wang Mengyao M Zheng Ya Y

Social cognitive and affective neuroscience 20190801 8

As a cardinal feature of several psychiatric disorders, anhedonia includes a consummatory component (deficits in hedonic response to rewards) and an anticipatory component (a reduced motivation to pursue them). Although being conceptualized as impairments of reward system, the neural characterization of reward processing in anhedonia is hampered by the enormous heterogeneity in the reward phase ('wanting' vs 'liking') and comorbidity (inherent to disease states). The current event-related potent ...[more]

PMID: 31506689

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Project description:Reward processing abnormalities have been implicated in the pathophysiology of negative symptoms such as anhedonia and avolition in schizophrenia. However, studies examining neural responses to reward anticipation and receipt have largely relied on instrumental tasks, which may confound reward processing abnormalities with deficits in response selection and execution. 25 chronic, medicated outpatients with schizophrenia and 20 healthy controls underwent functional magnetic resonance imaging using a pavlovian reward prediction paradigm with no response requirements. Subjects passively viewed cues that predicted subsequent receipt of monetary reward or non-reward, and blood-oxygen-level-dependent signal was measured at the time of cue presentation and receipt. At the group level, neural responses to both reward anticipation and receipt were largely similar between groups. At the time of cue presentation, striatal anticipatory responses did not differ between patients and controls. Right anterior insula demonstrated greater activation for nonreward than reward cues in controls, and for reward than nonreward cues in patients. At the time of receipt, robust responses to receipt of reward vs. nonreward were seen in striatum, midbrain, and frontal cortex in both groups. Furthermore, both groups demonstrated responses to unexpected versus expected outcomes in cortical areas including bilateral dorsolateral prefrontal cortex. Individual difference analyses in patients revealed an association between physical anhedonia and activity in ventral striatum and ventromedial prefrontal cortex during anticipation of reward, in which greater anhedonia severity was associated with reduced activation to money versus no-money cues. In ventromedial prefrontal cortex, this relationship held among both controls and patients, suggesting a relationship between anticipatory activity and anhedonia irrespective of diagnosis. These findings suggest that in the absence of response requirements, brain responses to reward receipt are largely intact in medicated individuals with chronic schizophrenia, while reward anticipation responses in left ventral striatum are reduced in those patients with greater anhedonia severity.

Project description:Ribot's (1896) long standing definition of anhedonia as "the inability to experience pleasure" has been challenged recently following progress in affective neuroscience. In particular, accumulating evidence suggests that reward consists of multiple subcomponents of wanting, liking and learning, as initially outlined by Berridge and Robinson (2003), and these processes have been proposed to relate to appetitive, consummatory and satiety phases of a pleasure cycle. Building on this work, we recently proposed to reconceptualize anhedonia as "impairments in the ability to pursue, experience, and/or learn about pleasure, which is often, but not always accessible to conscious awareness." (Rømer Thomsen et al., 2015). This framework is in line with Treadway and Zald's (2011) proposal to differentiate between motivational and consummatory types of anhedonia, and stresses the need to combine traditional self-report measures with behavioral measures or procedures. In time, this approach may lead to improved clinical assessment and treatment. In line with our reconceptualization, increasing evidence suggests that reward processing deficits are not restricted to impaired hedonic impact in major psychiatric disorders. Successful translations of animal models have led to strong evidence of impairments in the ability to pursue and learn about reward in psychiatric disorders such as major depressive disorder, schizophrenia, and addiction. It is of high importance that we continue to systematically target impairments in all phases of reward processing across disorders using behavioral testing in combination with neuroimaging techniques. This in turn has implications for diagnosis and treatment, and is essential for the purposes of identifying the underlying neurobiological mechanisms. Here I review recent progress in the development and application of behavioral procedures that measure subcomponents of anhedonia across relevant patient groups, and discuss methodological caveats as well as implications for assessment and treatment.

Project description:BackgroundAnhedonia, the diminished ability to experience pleasure, is an important dimensional entity linked to depression, schizophrenia, and other emotional disorders, but its origins and mechanisms are poorly understood. We have previously identified anhedonia, manifest as decreased sucrose preference and social play, in adolescent male rats that experienced chronic early-life adversity/stress (CES). Here we probed the molecular, cellular, and circuit processes underlying CES-induced anhedonia and tested them mechanistically.MethodsWe examined functional brain circuits and neuronal populations activated by social play in adolescent CES and control rats. Structural connectivity between stress- and reward-related networks was probed using high-resolution diffusion tensor imaging, and cellular/regional activation was probed using c-Fos. We employed viral-genetic approaches to reduce corticotropin-releasing hormone (Crh) expression in the central nucleus of the amygdala in anhedonic rats, and tested for anhedonia reversal in the same animals.ResultsSucrose preference was reduced in adolescent CES rats. Social play, generally considered an independent measure of pleasure, activated brain regions involved in reward circuitry in both control and CES groups. In CES rats, social play activated Crh-expressing neurons in the central nucleus of the amygdala, typically involved in anxiety/fear, indicating aberrant functional connectivity of pleasure/reward and fear circuits. Diffusion tensor imaging tractography revealed increased structural connectivity of the amygdala to the medial prefrontal cortex in CES rats. Crh-short hairpin RNA, but not control short hairpin RNA, given into the central nucleus of the amygdala reversed CES-induced anhedonia without influencing other emotional measures.ConclusionsThese findings robustly demonstrate aberrant interactions of stress and reward networks after early-life adversity and suggest mechanistic roles for Crh-expressing amygdala neurons in emotional deficits portending major neuropsychiatric disorders.

Project description:An inhibited neural response to reward is typical of clinical depression and can predict an individual's overall depressive symptoms. However, the mechanism underlying this are unclear. Previous studies have found that anhedonia and inattention may mediate the relationship between reward sensitivity and depressive symptoms. Therefore, this study aimed to verify the relationship between reward sensitivity and overall depressive symptoms in a depressive tendency sample as well as to explore the mechanism underlying the ability of neural responses to reward to predict overall depressive symptoms via a mediation model. Sixty-four participants (33 with depressive tendencies and 31 without; dichotomized by BDI-II) finished simple gambling tasks while their event-related potential components (ERPs) were recorded and compared. Linear regression was conducted to verify the predictive effect of ERPs on overall depressive symptoms. A multiple mediator model was used, with anhedonia and distractibility as mediators reward sensitivity and overall depressive symptoms. The amplitude of reward positivity (ΔRewP) was greater in healthy controls compared to those with depressive tendencies (p = 0.006). Both the gain-locked ERP component (b = - 1.183, p = 0.007) and the ΔRewP (b = - 0.991, p = 0.024) could significantly negatively predict overall depressive symptoms even after controlling for all anxiety symptoms. The indirect effects of anhedonia and distractibility were significant (both confidence intervals did not contain 0) while the direct effect of reward sensitivity on depressive symptom was not significant (lower confidence interval = - 0.320, upper confidence interval = 0.065). Individuals with depressive tendencies display impaired neural responses to reward compared to healthy controls and reduced individual neural responses to reward may reflect the different biotypes of depression such as anhedonia and inattention.

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Aberrant reward dynamics in trait anticipatory anhedonia.

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Aberrant reward dynamics in trait anticipatory anhedonia.

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