Cortico-Cardiac Processing of Affective-Motivational Cues - Mechanisms and Individual Differences
Several neurobiological models of emotion and personality assume basic neuropsychological systems in humans that are sensitive to affective, motivationally significant stimuli. Importantly, individuals are able to learn cue-stimulus associations that predict these motivational-affective stimuli. The...
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|Zusammenfassung:||Several neurobiological models of emotion and personality assume basic neuropsychological systems in humans that are sensitive to affective, motivationally significant stimuli. Importantly, individuals are able to learn cue-stimulus associations that predict these motivational-affective stimuli. The response to associated cues may not only include changes in subjective affective states (such as a feeling of joy or fear), but also physiological parameters like cardiac activity. Appropriate psychophysiological responding – such as defensive behavior in response to a threat cue or approach behavior in response to a reward cue – is evolutionary adaptive as it promotes survival of the individual and passing on of genes. It is argued that understanding mechanisms of motivational-affective cue processing is important to understand more complex phenomena of affective states and motivation, including affective personality traits and related psychopathologies. In the present thesis, we measured electroencephalography (EEG) indicators of central neural cue processing and cardiac indicators of subsequent behavioral adaptation. In addition, we computed intraindividual covariations of EEG and cardiac measures with the cardio-electroencephalographic covariance tracing method, to examine functional cortico-cardiac coupling. With this approach, we aimed to elucidate mechanisms of motivational-affective cue processing, including physiological-anatomical bases, temporal dynamics and long-term adaptation. In a gambling task in Study I, monetary win and loss feedback evoked intraindividual coupling of cortical and cardiac activity (indicated by the so-called N300H component), replicating previous results. Coupling was absent on trials where no money was at stake and feedback was not motivationally significant. In addition, analyses of brain structure involvement suggested the anterior cingulate cortex as a generator of coupling-related EEG and the insula as a moderator of cortico-cardiac coupling. In Study II, using the same gambling task as in Study I along with pharmacological manipulations, we showed that the neurotransmitters dopamine (which plays an important role in central feedback processing) and noradrenaline (which plays an important role in sympathetic cortico-cardiac transmission) are not associated with modulations of cortico-cardiac coupling in response to monetary win or loss feedback. Moreover, Study II replicated previous findings that the N300H is related to with trait anxiety. Finally, after a series of previous N300H replications, we conducted reliability and control analyses, which demonstrated statistically that the N300H is a robust marker of cortico-cardiac coupling. In Study III, participants underwent a two-day differential fear conditioning and extinction paradigm that allowed assessment of short-term conditioning and extinction on Day 1 of the paradigm, as well as recall indices of both non-extinguished and extinguished fear on Day 2. First, we showed that cortico-cardiac coupling is evoked in response to threat stimuli, generalizing findings from the previous gambling paradigm. Second, we found that cortico-cardiac coupling was evoked by cues that have acquired motivational significance via conditioning, whereas cortico-coupling had been evoked by instructed feedback cues in the previous two studies. Notably, coupling disappeared after fear extinction but was still present in non-extinguished fear stimuli one day after initial learning, indicating long-term stability of conditioned cortico-cardiac coupling. Regarding univariate measures, we showed for the first time that the late positive potential – a component in the EEG that is sensitive to motivational stimulus significance – is modulated not only in inherently threatening stimuli but also in conditioned threat stimuli. In addition, we showed long-term stability of cardiac slowing to conditioned threat stimuli (‘fear bradycardia’), which was still present during Day 2 testing. In Study IV, using the same paradigm as in Study III, we investigated the role of genes and personality in short-term and long-term fear conditioning and extinction. We found that the dopaminergic Val158Met polymorphism on the catechol-o-methyltransferase gene predicted long-term conditioned and extinguished fear responses in both the late positive potential and fear bradycardia. Moreover, we found that trait fearfulness is a superior predictor of the magnitude of fear bradycardia during conditioning than are widely used measures of neuroticism/anxiety. Meanwhile, we suggested high levels of neuroticism/anxiety as a predictor of unstable, maladaptive long-term retention of extinguished fear bradycardia. Taken together, the present thesis was able to elucidate mechanisms of motivational-affective cue processing, cardiac adaptation and both short-term and long-term learning. Findings were discussed in terms of their generalizability and implications for psychophysiological models of affect, motivation, personality, and psychopathology.|