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Sleep Spindles Gate the Temporal Window for Emotional Memory Modification

Poster Session E - Monday, March 9, 2026, 2:30 – 4:30 pm PDT, Fairview/Kitsilano Ballroom
Also presenting in Data Blitz Session 3 - Saturday, March 7, 2026, 10:30 am – 12:00 pm PST, Salon E.

Tao Xia¹, Xiaoqing Hu²; ¹The University of Hong Kong

Targeted memory reactivation (TMR) during sleep offers a promising, non-invasive avenue for modifying unwanted aversive memories, purportedly by reopening a window of memory lability. We directly tested this hypothesis by investigating whether TMR during NREM sleep allows external stimuli to disrupt memory stabilization. Across two experiments, we reactivated aversive memories with auditory cues during NREM sleep, followed by positive-word interference. Experiment 1 revealed a critical behavioral window: interference delivered 2s or 4s post-cue significantly impaired subsequent memory recall compared to 1s (1s vs. 2s: z=3.048, p=.007; 1s vs. 4s: z=2.292, p=.033). A preregistered second experiment then clarified the functional nature of this disruption. While cueing alone successfully enhanced memory retention (cued vs. uncued: z=2.685, p=0.022), the addition of interference completely nullified this TMR benefit, returning memory performance to the level of uncued items (cued+interference vs. uncued: z=1.535, p=.125; cued+interference vs. cued: z=1.759, p=.118). Crucially, sleep EEG analyses revealed that these behavioral outcomes are governed by the real-time dynamics of cue-induced sleep spindles. Across both experiments, the timing of interference relative to the spindle robustly predicted memory outcome (Exp1: z=-2.117, p=.034; Exp2: z=-2.47, p=.014). Specifically, interference delivered after a spindle was significantly more detrimental to memory than interference delivered during a spindle (Exp1: z=-3.019, p=.004; Exp2: z=-2.702, p=.021). Our findings demonstrate the window for memory modification is not merely temporal, but is gated by the brain's intrinsic neurophysiological event. This provides a neurodynamic mechanism to decouple memory reactivation from its subsequent reinforcement, offering a promising therapeutic target.

Topic Area: LONG-TERM MEMORY: Episodic