Dopaminergic modulation of stress-induced alterations in goal-directed behaviour and associated brain activation
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Abstract
Being exposed to acute stress may cause people to behave more habitual, which purportedly is associated stress-induced increased dopamine release. In contrast, experimental rises in systemic dopamine levels have been shown to increase goal-directed behaviour and, thus, decrease habitual control. Whether experimentally increased dopamine functioning can modulate stress-induced reductions in goal-directed behaviour and its neural substrates, is currently unknown. To assess whether increased dopamine functioning reduces stress effects on goal-directed behaviour, 100 participants were recruited who were randomly assigned to one of four conditions in a 2x2 between participants design. Participants underwent a stress induction protocol (Maastricht Acute Stress Test; MAST) or a control procedure and received methylphenidate (40 mg, oral) or placebo. In a well-established instrumental learning paradigm, participants were trained to learn stimulus-response-outcome associations, after which rewards were selectively devalued and participants’ goal-directed behaviour was assessed at peak cortisol/methylphenidate concentrations in a magnetic resonance imaging scanner to assess brain activation. The MAST effectively increased physiological measures of stress (salivary cortisol, blood pressure) and subjective stress. Methylphenidate also increased cortisol levels over time. While stress selectively reduced goal-directed behaviour, this effect was not modulated by methylphenidate. However, methylphenidate modulated stress effects on activation in paracingulate, orbitofrontal cortex, and anterior cingulate associated with expected value representation in goal-directed behaviour. Our neuroimaging data suggest increased dopamine levels reverse stress-induced changes in brain activation associated with goal-directed behaviour. These effects may be relevant for preventing stress-induced relapse in addictive behaviour.
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