Post-loss speeding and neurophysiological markers of action preparation and outcome processing in probabilistic reversal learning

Losses and errors often slow down subsequent reaction times (RTs). This is classically explained in terms of a shift towards more cautious, therefore slow, behaviour. Recent studies of gambling, however, reported faster RTs following losses, so-called post-loss speeding , often attributing these to...

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Bibliographic Details
Published inQuarterly journal of experimental psychology (2006) p. 17470218251333429
Main Authors Kulakova, Eugenia, Majchrowicz, Bartosz, Saydam, Şiir Su, Haggard, Patrick
Format Journal Article
LanguageEnglish
Published England 02.04.2025
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Summary:Losses and errors often slow down subsequent reaction times (RTs). This is classically explained in terms of a shift towards more cautious, therefore slow, behaviour. Recent studies of gambling, however, reported faster RTs following losses, so-called post-loss speeding , often attributing these to behavioural impulsivity arising from frustration. Here we instead investigated post-loss speeding in the context of a task that allowed behavioural adaptation and learning, namely probabilistic reversal learning (PRL). We additionally used electroencephalography (EEG) to investigate how losses influence subsequent markers of action generation (readiness potential [RP]) and outcome evaluation (feedback-related negativity [FRN] and P300). Our results confirm faster RTs after losses than after wins in PRL, thus extending post-loss speeding from gambling to cognitive contexts where learning is possible. Previous losses did not affect subsequent RP amplitudes. However, compared to wins, previous losses led to more positive FRN and more positive P300 amplitudes elicited by subsequent outcomes. Furthermore, faster RTs were associated with more negative FRN amplitudes irrespective of previous or outcome valence. We hypothesise that post-loss speeding in PRL may represent a form of signal chasing, allowing participants to behaviourally modulate neurophysiological responses and thereby potentially establish agency by influencing internal neurophysiological signals.
ISSN:1747-0218
1747-0226
DOI:10.1177/17470218251333429