Abstract

Background:Acute stress is thought to reduce goal-directed behaviour, an effect purportedly associated with stress-induced release of catecholamines. In contrast, experimentally increased systemic catecholamine levels have been shown to increase goal-directed behaviour. Whether experimentally increased catecholamine function can modulate stress-induced reductions in goal-directed behaviour and its neural substrates, is currently unknown.Aim:To assess whether and how experimentally induced increases in dopamine and noradrenaline contribute to the acute stress effects on goal-directed behaviour and associated brain activation.Methods:One hundred participants underwent a stress induction protocol (Maastricht acute stress test; MAST) or a control procedure and received methylphenidate (MPH) (40 mg, oral) or placebo according to a 2 × 2 between-subjects design. In a well-established instrumental learning paradigm, participants learnt stimulus–response–outcome associations, after which rewards were selectively devalued. Participants’ brain activation and associated goal-directed behaviour were assessed in a magnetic resonance imaging scanner at peak cortisol/MPH concentrations.Results:The MAST and MPH increased physiological measures of stress (salivary cortisol and blood pressure), but only MAST increased subjective measures of stress. MPH modulated stress effects on activation of brain areas associated with goal-directed behaviour, including insula, putamen, amygdala, medial prefrontal cortex, frontal pole and orbitofrontal cortex. However, MPH did not modulate the tendency of stress to induce a reduction in goal-directed behaviour.Conclusion:Our neuroimaging data suggest that MPH-induced increases in dopamine and noradrenaline reverse stress-induced changes in key brain regions associated with goal-directed behaviour, while behavioural effects were absent. These effects may be relevant for preventing stress-induced maladaptive behaviour like in addiction or binge eating disorder.

Highlights

  • Stress plays an important role in the development and maintenance of maladaptive behaviours like addiction (Brewer et al, 1998; Sinha, 2001; Sinha and Jastreboff, 2013)

  • Conservative power analyses (GPower; Faul et al, 2007: α = 0.05 two-tailed; 1 − β = 0.80) based on previous effects size of MAST observed in our previous studies in a 2 (MAST: stress and control) × 2 (Value: valuable, devalued) repeated measure design (η2p = 0.10; Smeets et al, 2019), indicate that the required sample size is 80 participants

  • Elevated cortisol levels were observed following the MAST in the stress relative to the control condition until 75 min after the stress induction (MAST × time: F(2.898,255.003) = 3.26, p = 0.023 η2p = 0.036)

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Summary

Introduction

Stress plays an important role in the development and maintenance of maladaptive behaviours like addiction (Brewer et al, 1998; Sinha, 2001; Sinha and Jastreboff, 2013). Acute stress is thought to reduce goal-directed behaviour, an effect purportedly associated with stress-induced release of catecholamines. Whether experimentally increased catecholamine function can modulate stress-induced reductions in goal-directed behaviour and its neural substrates, is currently unknown. Aim: To assess whether and how experimentally induced increases in dopamine and noradrenaline contribute to the acute stress effects on goaldirected behaviour and associated brain activation. Conclusion: Our neuroimaging data suggest that MPH-induced increases in dopamine and noradrenaline reverse stress-induced changes in key brain regions associated with goal-directed behaviour, while behavioural effects were absent. These effects may be relevant for preventing stress-induced maladaptive behaviour like in addiction or binge eating disorder

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