Active forgetting explains the intrinsic instability of a labile memory lasting for hours. However, how such memory maintains stability against unwanted disruption is not completely understood. Here, we report a learning-activated active protection mechanism that enables labile memory to resist disruptive sensory experiences in Drosophila. Aversive olfactory conditioning activates mitogen-activated protein kinase (MAPK) transiently in the mushroom-body γ lobe, where labile-aversive memory is stored. This increased MAPK activity significantly prolongs labile memory retention and enhances its resistance to disruption induced by heat shock, electric shock, or odor reactivation. Such experience-induced forgetting cannot be prevented by inhibition of Rac1 activity. Instead, protection of Rac1-independent forgetting correlates with non-muscle myosin II activity and persistence of learning-induced presynaptic structural changes. Increased Raf/MAPK activity, together with suppressed Rac1 activity, completely blocks labile memory decay. Thus, learning not only leads to memory formation, but also activates active protection and active forgetting to regulate the formed memory.

中文翻译：

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主动保护：学习激活的Raf / MAPK活性可以保护不稳定的记忆，使其免受Rac1独立的遗忘。

主动遗忘解释了持续数小时的不稳定内存的内在不稳定性。但是，这种存储器如何保持稳定性以防止不必要的破坏还没有被完全理解。在这里，我们报告了一种学习激活的主动保护机制，该机制可使不稳定的记忆抵抗果蝇中的破坏性感官体验。厌恶性嗅觉调节会在蘑菇体γ瓣中暂时激活有丝分裂原活化的蛋白激酶（MAPK），该处存储了不稳定的平均记忆。这种增加的MAPK活性显着延长了不稳定的记忆力，并增强了其抵抗由热休克，电击或气味再激活引起的破坏的能力。不能通过抑制Rac1活性来防止这种经验引起的遗忘。反而，Rac1依赖性遗忘的保护与非肌肉肌球蛋白II活性和学习诱导的突触前结构变化的持久性相关。增加的Raf / MAPK活性，以及​​抑制的Rac1活性，完全阻止了不稳定的记忆衰退。因此，学习不仅导致记忆形成，而且激活主动保护和主动遗忘来调节形成的记忆。