Modulating emotional attentional bias through targeted memory reactivation during sleep: Preliminary data

Introduction: Attentional Bias (AB) is the tendency among individuals with emotional dysregulation to preferentially allocate attention toward negative emotional stimuli rather than positive ones, influencing the encoding and consolidation of emotional events. Targeted Memory Reactivation (TMR) holds promise in memory enhancement by reactivating specific memory traces during sleep. We aimed to explore the potential of TMR in modulating AB. Methods: Eighteen females (mean age ± standard deviation, 21.56 ± 2.04) participated in a between-subjects design. AB was assessed using a modified Dot-Probe Task (DPT) before (T1) and after (T2) a nocturnal sleep with acoustic stimulation (TMR vs. Control) during slow-wave sleep (SWS). During DPT, participants viewed pairs of emotional faces (positive/negative) followed by a probe. They indicated the probe's position (left/right) while simultaneously being exposed to a specific auditory cue, one for positive and one for negative image-probe association (positive valence/negative valence). During sleep, the TMR group was exposed to the sound associated with the positive valence of the DPT, while a novel sound was presented to the Control group. To assess the effect of the acoustic stimulation during sleep, mixed ANOVA was applied to the reaction times (RTs) of the DPT, with valence (positive/negative), session (T1/T2), and group (TMR/Control) as within/between factors. To evaluate the EEG correlates of TMR, unpaired t-tests were employed comparing ERPs between TMR and Control groups in terms of amplitude and timefrequency analysis. Results: ANOVA on RTs showed a significant effect of the session factor (p = 0.02), with a general reduction in RTs at T2. The EEG correlates of nocturnal stimulation revealed a higher ERP amplitude  1000 post-stimulation at the frontal site (p < 0.01). Concurrently, timefrequency analysis highlighted an increased slow spindle activity in the frontal and central regions (all p < 0.01)  1000 ms poststimulation. Conclusion: TMR does not seem to modulate AB in healthy subjects, although it appears to reactivate declarative memory traces, as indicated by increased ERP amplitudes and spindle activity. These findings suggest that the implicit memory process underlying AB modification, potentially independent from hippocampal processes, is not susceptible to modulation through TMR during SWS.