After an event takes place, we may memorize different aspects of the experience, such as visual details or the general context. Empirically, these memory components appear to fade away at different rates, suggesting different cellular and/or molecular mechanisms underlying such memory decay. Drosophila, a pioneering animal model for discovering genetic components of forgetting, is known to form at least 2 different memory components after learning: anesthesia-sensitive memory (ASM) and anesthesia-resistant memory (ARM) (1). These 2 memory components are distinguishable from each other behaviorally and genetically (2⇓–4), but both show decremental forgetting. Interestingly, the decay rates of ASM and ARM depend on 2 different Rho family proteins (5, 6). An important question is what signal cascades are downstream of these GTPases. Gao et al. (7) connect the dots by discovering distinct actin remodeling mechanisms for forgetting of ASM and ARM. Forgetting opposes memory formation. Intuitively, people think that forgetting is a passive process—memory gradually fades away just as a rock is eroded over time and loses its shape. For an efficient information storage system to work properly, however, a dedicated “delete” function which removes unused or inappropriate information is required. From a molecular perspective, variant kinases and receptors are phosphorylated after learning, and the process is required for maintenance of labile memory (8). With time, basal activity of phosphatase within the neuron may counteract the learning-induced phosphorylation (9), thus “passively” …
Date:
2019-10
Relation:
Proceedings of the National Academy of Sciences of the United States of America. 2019 Oct;116(42):20807-20808.
