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Anhedonia modulates the effects of positive mood induction on reward-related brain activation.

ABSTRACT: Blunted activation in the reward circuitry has been associated with anhedonia, the inability to experience pleasure in previously rewarding activities. In healthy individuals, reward-related activation has been found to be modulated by acute contextual factors such as induced positive mood. Accordingly, blunted reward response in anhedonia might involve a failure to appropriately modulate reward-related activation as a function of context. To test this hypothesis, 29 participants (19 females, mean age of 24.14?±?4.61, age range 18-34), with a wide range of anhedonic symptoms, underwent functional MRI while anticipating and receiving monetary rewards, before and after a positive mood induction. Change in neural activation from before to after mood induction was quantified, and effects of anhedonia were investigated through whole-brain, ROI, and functional connectivity analyses. Contrary to hypotheses, results indicated that during reward anticipation (but not receipt), nucleus accumbens activation decreased while its connectivity with the dorsolateral prefrontal cortex increased, following positive mood induction. Critically, anhedonia modulated both effects. The unexpected finding of decreased activation to reward cues following positive mood induction is compelling as it aligns with a prominent behavioral model of the effect of positive mood on exploration of rewarding and neutral stimuli. Furthermore, the modulation of this effect by anhedonia suggests that it may be a key process altered in anhedonia.

SUBMITTER: Green IW

PROVIDER: S-EPMC6813811 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature

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Anhedonia modulates the effects of positive mood induction on reward-related brain activation.

Green Isobel W IW Pizzagalli Diego A DA Admon Roee R Kumar Poornima P

NeuroImage 20190301

Blunted activation in the reward circuitry has been associated with anhedonia, the inability to experience pleasure in previously rewarding activities. In healthy individuals, reward-related activation has been found to be modulated by acute contextual factors such as induced positive mood. Accordingly, blunted reward response in anhedonia might involve a failure to appropriately modulate reward-related activation as a function of context. To test this hypothesis, 29 participants (19 females, me ...[more]

PMID: 30831312

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Project description:Cocaine exhibits high liability for inducing addictive behaviors, but the mechanisms of neuroplasticity underlying the behavioral effects remain unclear. As a crucial mediator of neuroplasticity in diverse functional models, brain-derived neurotrophic factor (BDNF) could contribute to the mechanisms of addiction-related neuroplasticity. Here, we addressed the hypothesis that cocaine increases synaptic dopamine, which induces BDNF protein expression to initiate addiction-related behavior in the rat. An enzyme-linked immunosorbent assay was used to measure BDNF protein expression in rat striatal tissues. For behavioral readout, we used a noninvasive measurement system to measure the emission of 50-kHz ultrasonic vocalization (USV), a response that correlates with electrical brain stimulation and conditioned place preference behavior in rodents. A single injection of cocaine significantly increased BDNF protein expression, but this effect was not further augmented by repeated cocaine administration. A single administration of cocaine elicited significant and dose-related USV responses, and the magnitude of the behavior increased with repeated drug administration. R-(+)-7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine (SCH23390), but not raclopride, significantly attenuated cocaine-induced BDNF protein expression, whereas either the D(1)-like or D(2)-like receptor antagonist blocked cocaine-induced USV behavior. Furthermore, significant USV behavior was elicited by the nonselective dopamine agonist, apomorphine, but not by agonists that are selective for D(1)-like or D(2)-like receptors. Intracerebroventricular injection of the neurotrophin TrkB receptor inhibitor, K252a, blocked cocaine-induced USV behavior but not locomotor activity. These results suggest that neurotrophin signaling downstream of dopamine receptor function probably constitutes a crucial link in cocaine induction of USV behavior and may contribute to the mechanisms underlying the development of addiction-related behaviors.

Dataset Information

Anhedonia modulates the effects of positive mood induction on reward-related brain activation.

Publications

Anhedonia modulates the effects of positive mood induction on reward-related brain activation.

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