Inflammation and dimensions of reward processing following exposure to the influenza vaccine

Boyle, Chloe C.; Kuhlman, Kate R.; Dooley, Larissa N.; Haydon, Marcie D.; Robles, Theodore F.; Ang, Yuen‐Siang; Pizzagalli, Diego A.; Bower, Julienne E.

doi:10.1016/j.psyneuen.2018.11.024

Cited by 33 publications

(32 citation statements)

References 67 publications

(102 reference statements)

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“…Three studies have used the EEfRT and all found a different pattern. The current study found stress-induced inflammation increased motivation for low probability trials, endotoxin has been shown to increase motivation for high probability trials (Lasselin et al, 2016) and influenza vaccination was associated with a global decrease in motivation regardless of probability (Boyle et al, 2018). Using an 'effortstake task' that does not alter probability, Draper and colleagues (2018) found a reduction in motivation following endotoxin in a sample of healthy men.…”

Section: Discussionmentioning

confidence: 53%

“…Given this background, enhanced reward responsiveness and motivation in association with the stress-induced inflammatory response was unexpected. The rapidly expanding literature on inflammation and reward suggests a complicated relationship that may vary as a function of reward dimension (e.g., motivation vs. sensitivity; Draper et al, 2018;Lasselin et al, 2016;Dantzer et al, 2014), reward type (e.g., monetary vs social; Inagaki et al, 2015), level of analysis (e.g., neuroimaging vs. behavior; 26), and the magnitude of the inflammatory response (e.g., endotoxin vs. vaccination; Lasselin et al, 2016;Boyle et al, 2018). In addition, effects of stress and inflammation on reward in human models have previously been examined in isolation, but stress-induced inflammation involves a different psychological and physiological experience.…”

Section: Discussionmentioning

confidence: 99%

“…2.2.1. Inflammation-Circulating concentrations of the pro-inflammatory cytokine IL-6 were used to measure inflammation because IL-6 increases following the TSST (Marsland et al, 2017), is elevated in individuals with depression (Haapakoski et al, 2015), and is associated with changes in reward processing and/or mood following an inflammatory stimulus (Lasselin et al, 2016;Boyle et al, 2018;Kuhlman et al, 2018). Blood samples were collected by venipuncture into ethylene diamine tetraacetic acid tubes, placed on ice, centrifuged for acquisition of plasma and stored at −80 °C.…”

Section: Methodsmentioning

confidence: 99%

“…with prior work and current recommendations (e.g., Bogdan and Pizzagalli, 2006;Boyle et al, 2018;Pizzagalli et al, 2005;Pechtel et al, 2015), PRT data was cleaned using the following established inclusion criteria for evaluable data: accuracy greater than 50%; ratio of rewards received greater than 2.4; at least 80% trials within valid range (150 ms-2500 ms); < 16 outliers (after log transformation, trials with reaction times falling outside the mean +/− 3 standard deviations were considered outliers). Ten participants were excluded (18.5% of the sample) leaving a total of 44 participants (n = 31 stress).…”

Section: Task Analyses: Prt-consistentmentioning

confidence: 99%

“…Stress is a well-established and robust predictor of depression onset and recurrence (Kendler et al, 2003;Monroe and Reid, 2009;Hammen, 2015) and is linked specifically with alterations in reward-related processes (Cavanagh et al, 2010;Porcelli et al, 2012;Treadway et al, 2013;Harrison et al, 2016;Harrison et al, 2015;Capuron et al, 2012;Draper et al, 2018;Lasselin et al, 2016;Boyle et al, 2018). Stress also leads to increases in inflammation, which may be a critical pathway linking stress and reward dysregulation.…”

Section: Introductionmentioning

confidence: 99%

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Effects of stress-induced inflammation on reward processing in healthy young women

Boyle

Stanton

Eisenberger

et al. 2020

Brain, Behavior, and Immunity

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Background-Anhedonia, or loss of interest or pleasure, is a feature of depression and transdiagnostic construct in psychopathology. Theory and compelling evidence from preclinical models implicates stress-induced inflammation as a psychobiological pathway to anhedonic behavior; however, this pathway has not been tested in human models. Further, although anhedonia may reflect dysregulation in multiple dimensions of reward, the extent to which stressinduced inflammation alters these dimensions is unclear. Thus, the current experimental study used a standardized laboratory stressor task to elicit an inflammatory response and evaluate effects of stress-induced inflammation on multiple behavioral indices of reward processing. Methods-Healthy young women (age 18-25) completed behavioral reward tasks assessing reward learning, motivation, and sensitivity and were randomized to undergo an acute psychosocial stressor (n = 37) or a nostress active control (n = 17). Tasks were re-administered 90-120min post-stress to coincide with the peak of the stress-induced inflammatory response. Blood samples were collected for assessment of the pro-inflammatory cytokine interleukin-6 (IL-6) at baseline and 90 and 120 min post stressor.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Task Analyses: Prt-consistentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Effects of stress-induced inflammation on reward processing in healthy young women

Boyle

Stanton

Eisenberger

et al. 2020

Brain, Behavior, and Immunity

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Neurobiology, Clinical Presentation, and Treatment of Methamphetamine Use Disorder

2020

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In the wake of the opioid crisis, methamphetamine has reemerged as a challenge to mental health clinicians and researchers alike. Methamphetamine is now available in different forms such as ice, powder, and pills, with different pharmacokinetic characteristics that make them popular among certain types of individuals. 1 Recent seizure data suggest that methamphetamine production and trafficking are spreading into new areas of the globe. 2 According to the Automation of Reports and Consolidated Orders System, methamphetamine consumption increased 4-fold between 2015 and 2016 and total stimulant use doubled in the last decade. 3 From 2011 through 2016, the age-adjusted rate of drug overdose deaths involving methamphetamine more than tripled. 4 Moreover, drug overdose deaths involving cocaine, amphetamines, or both substances combined increased 42.4% from 12 122 in 2015 to 17 258 in 2016. 5 Based on the most recent data from the National Survey on Drug Use and Health, 6 the 12-month prevalence of individuals aged 12 years or older reporting methamphetamine use has increased by 195% from its low in 2010 to 2018 (Figure 1), and it is estimated that 1.86 million Americans used methamphetamine in 2018. These numbers underline the importance of paying attention to the possibility of the next substance use crisis. However, whereas opioid use disorder can be treated pharmacologically 7 and behaviorally, 8 there are significant challenges for the treatment of methamphetamine use disorder (MUD). This review focuses on 3 specific aspects of MUD. First, the neurobiology of methamphetamine is more complex than the traditional view of it as a monoaminergic modulator. Second, the clinical presentation is not limited to the symptoms associated with use disorder but extend to medical presentations, most notably the cardiovascular and cerebrovascular systems. Third, pharmacologic interventions focused on modulating the monoaminergic pathways have largely failed, and new pharmacologic approaches are necessary to focus on novel treatment targets. In the final section, several suggestions will be proposed for both clinicians and researchers to advance the understanding of MUD. Biological Pathways, Neural Basis, and CognitionMethamphetamine has been conceptualized primarily as a releaser of dopamine, serotonin, noradrenaline, and adrenaline from nerve terminals in the central and peripheral nervous system, 9 which occurs via several different mechanisms, including (1) redistributing catecholamines from synaptic vesicles to the cytosol, (2) reversing the plasma membrane transport of neurotransmitters, (3) blocking the activity of monoamine transporters, (4) decreasing the expression of dopamine transporters at the cell surface, (5) inhibiting monoamine oxidase activity, and (6) increasing the activity and IMPORTANCE The prevalence of and mortality associated with methamphetamine use has doubled during the past 10 years. There is evidence suggesting that methamphetamine use disorder could be the next substance use crisis in the United ...

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Inflammation as a Pathophysiologic Pathway to Anhedonia: Mechanisms and Therapeutic Implications

Bekhbat

Treadway

Felger

2022

Anhedonia: Preclinical, Translational, and Clinical Integration

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Inflammation and dimensions of reward processing following exposure to the influenza vaccine

Cited by 33 publications

References 67 publications

Effects of stress-induced inflammation on reward processing in healthy young women

Effects of stress-induced inflammation on reward processing in healthy young women

Neurobiology, Clinical Presentation, and Treatment of Methamphetamine Use Disorder

Inflammation as a Pathophysiologic Pathway to Anhedonia: Mechanisms and Therapeutic Implications

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