Cdc42-Dependent Forgetting Regulates Repetition Effect in Prolonging Memory Retention.
By Xuchen Zhang, Qian Li, Lianzhang Wang, Zhong-Jian Liu, Yi Zhong. 2016
43 citations recorded by the source corpus.
Repeated learning is used daily and is a powerful way to improve memory. A fundamental question is how multiple learning trials add up to improve memory. While the major studies so far of such a repetition effect have emphasized the strengthening of memory formation, the current study reveals a molecular mechanism through suppression of forgetting. We find that single-session training leads to formation of anesthesia-resistant memory (ARM) and then activation of the small G protein Cdc42 to cause decay or forgetting of ARM within 24 hr. Repetition suppresses the activation of Cdc42-dependent forgetting, instead of enhancing ARM formation, leading to prolonged ARM. Consistently, inhibition of Cdc42 activity through genetic manipulation mimicked the repetition effect, while repetition-induced ARM improvement was abolished by elevated Cdc42 activity. Thus, only the first session in repetitive training contributes to ARM formation, while the subsequent sessions are devoted not to acquiring information but to inhibiting forgetting.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Molecular Biology
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Citations in the corpus
- Genetic dissection of mutual interference between two consecutive learning tasks in Drosophila (2022, background): “After 20 min, the memory performance of the proactive task partially declines and a consolidated memory component called anesthesiaresistant memory (ARM) is largely formed (Quinn and Dudai, 1976; Tully et al., 1994; Tully and Quinn, 1985; Zhang et al., 2016).”
- Genetic dissection of active forgetting in labile and consolidated memories in Drosophila (2019, methodology): “Consistent with our previous finding (4), flies expressing constitutively active Cdc42 (MB-GS/UAS-Cdc42-CA, RU486+) had reduced ARM performance at 9 h after a 1-session training when compared with control flies (MB-GS/+, RU486+).”
- The Biology of Forgetting – A Perspective (2017, background): “Aswith Rac1-dependent forgetting, the activity ofCdc42 is increasedbyconditioning, such that conditioning promotesbothacquisitionand forgetting.”
- Active Protection: Learning-Activated Raf/MAPK Activity Protects Labile Memory from Rac1-Independent Forgetting. (2018, unknown): “Associative experiences such as interference and reversal learning act through active forgetting to accelerate memory decay (Cervantes-Sandoval et al., 2016; Liu et al., 2016b; Shuai et al., 2010; Zhang et al., 2016).”