Consolidated memories may return to labile/unstable states after their reactivation, thus requiring a restabilization process that is known as reconsolidation. During this time-limited reconsolidation window, reactivated existing memories can be strengthened, weakened or updated with new information. Previous studies have shown that noninvasive stimulation of the lateral prefrontal cortex after memory reactivation strengthened existing verbal episodic memories through reconsolidation, an effect documented by enhanced delayed memory recall (24h post-reactivation). However, it remains unknown whether the left posterior parietal cortex (PPC), a region involved during reactivation of existing episodic memories, contributes to reconsolidation. To address this question, in this double-blind experiment healthy participants (n=27) will receive transcranial direct current stimulation (tDCS) with the anode over the left PPC after reactivation of previously learned verbal episodic memories. Memory recall will be tested 24h later. To rule out unspecific effects of memory reactivation or tDCS alone, we will include two control groups: one that receives tDCS with the anode over the left PPC without reactivation (n=27) and another one that receives tDCS with the anode over a control site (primary visual cortex) after reactivation (n=27). We hypothesize that tDCS with the anode over the left PPC after memory reactivation will enhance delayed recall through reconsolidation relative to the two control groups. Knowledge about the critical nodes of the episodic memory reconsolidation network may help develop effective interventions to modulate existing memories in patients with memory disorders.
Consolidated memories may return to labile/unstable states after their reactivation, thus requiring a restabilization process that is known as reconsolidation. During this time-limited reconsolidation window, reactivated existing memories can be strengthened, weakened or updated with new information. Previous studies have shown that non-invasive stimulation of the lateral prefrontal cortex after memory reactivation strengthened existing verbal episodic memories through reconsolidation, an effect documented by enhanced delayed memory recall (24 h post-reactivation). However, it remains unknown whether the left posterior parietal cortex (PPC), a region involved during reactivation of existing episodic memories, contributes to reconsolidation. To address this question, in this double-blind experiment healthy participants (n = 27) received transcranial direct current stimulation (tDCS) with the anode over the left PPC after reactivation of previously learned verbal episodic memories. Memory recall was tested 24 h later. To rule out unspecific effects of memory reactivation or tDCS alone, we included two control groups: one that receives tDCS with the anode over the left PPC without reactivation (n = 27) and another one that receives tDCS with the anode over a control site (primary visual cortex) after reactivation (n = 27). We hypothesized that tDCS with the anode over the left PPC after memory reactivation would enhance delayed recall through reconsolidation relative to the two control groups. No significant between groups differences in the mean number of words recalled on day 3 occurred, suggesting no beneficial effect of tDCS over the left PPC. Alternative explanations were discussed, including efficacy of tDCS, different stimulation parameters, electrode montage, and stimulation site within the PPC.