Abstract
External and internal performance feedback triggers neural and visceral modulations such as reactions in the medial prefrontal cortex and insulae or changes of heart period (HP). The functional coupling of neural and cardiac responses following feedback (cortico-cardiac connectivity) is not well understood. While linear time-lagged within-subjects correlations of single-trial EEG and HP (cardio-electroencephalographic covariance tracing, CECT) indicate a robust negative coupling of EEG magnitude 300 ms after presentation of an external feedback stimulus with subsequent alterations of heart period (the so-called N300H phenomenon), the neurotransmitter systems underlying feedback-evoked cortico-cardiac connectivity are largely unknown. Because it has been shown that acute tryptophan depletion (ATD), attenuating brain serotonin (5-HT), decreases cardiac but not neural correlates of feedback processing, we hypothesized that 5-HT may be involved in feedback-evoked cortico-cardiac connectivity. In a placebo-controlled double-blind cross-over design, 12 healthy male participants received a tryptophan-free amino-acid drink at one session (TRP−) and a balanced amino-acid control-drink (TRP+) on another and twice performed a time-estimation task with feedback presented after each trial. N300H magnitude and plasma tryptophan levels were assessed. Results indicated a robust N300H after TRP+, which was significantly attenuated following TRP−. Moreover, plasma tryptophan levels during TRP+ were correlated with N300H amplitude such that individuals with lower tryptophan levels showed reduced N300H. Together, these findings indicate that 5-HT is important for feedback-induced covariation of cortical and cardiac activity. Because individual differences in anxiety have previously been linked to 5-HT, cortico-cardiac coupling and feedback processing, the present findings may be particularly relevant for futures studies on the relationship between 5-HT and anxiety.
Highlights
We rapidly process internal and external feedback signals in order to optimally interact with our environment
Central 5-HT was manipulated through administration of drinks that either contained no tryptophan (TRP−), serving to deplete this precursor of 5-HT synthesis, or elevated tryptophan levels (TRP+) in two separate sessions
Five hours later, when plasma levels of tryptophan were reduced in the TRP− vs. TRP+ session, participants conducted a time estimation task in which feedback was given after each trial
Summary
We rapidly process internal and external feedback signals in order to optimally interact with our environment. Neural signatures of error or negative feedback processing (e.g., event-related potentials, fMRI activation) are often accompanied by changes of behavior (Debener et al, 2005; Eichele et al, 2010; Mueller et al, 2011): the commission of an error in a speeded reaction time task can lead to subsequent slowing of reaction times; the presentation of negative feedback following a particular decision can alter decision-making in the future The adaptiveness of such behavioral changes with regard to task performance is still under investigation (Notebaert et al, 2009). Because these peripheral reactions are sensitive to feedback valence, even in the case of abstract feedback stimuli, which can hardly be adequately represented at the subcortical level, it is likely that cortical structures are involved in the modulation of cardiac responses at some point
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