Recovery of "Lost" Infant Memories in Mice
Recovery of "Lost" Infant Memories in Mice
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DOI：
10.1016/j.cub.2018.05.059
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发表时间：
2018-07-23
期刊：
影响因子：
9.2
通讯作者：
Frankland, Paul W.
中科院分区：
文献类型：
--
作者：
Guskjolen, Axel;Kenney, Justin W.;Frankland, Paul W.
人类和非人类动物在婴儿期形成的依赖海马体的事件相关记忆很快就会被遗忘。最近我们发现，高水平的海马体神经发生有助于加快婴儿期的遗忘速度。在这里，我们要问的是，这些在婴儿时期形成的记忆是否会被永久地抹去（即存储失败），或者随着时间的推移逐渐变得难以访问（即检索失败）。为此，我们开发了一种光遗传策略，使我们能够在幼鼠的情境恐惧编码过程中激活的神经元群中永久表达通道视紫红质-2 （ChR2）。然后，我们询问齿状回中chr2标记的集合的重新激活是否足以恢复成年期的记忆。我们发现，在训练后3个月，标记的齿状回神经元的光遗传刺激恢复了“丢失”的婴儿记忆，并且记忆恢复与标记的海马和皮层神经元群的更广泛的再激活有关。
Hippocampus-dependent, event-related memories formed in early infancy in human and non-human animals are rapidly forgotten. Recently we found that high levels of hippocampal neurogenesis contribute to accelerated rates of forgetting during infancy. Here, we ask whether these memories formed in infancy are permanently erased (i.e., storage failure) or become progressively inaccessible with time (i.e., retrieval failure). To do this, we developed an optogenetic strategy that allowed us to permanently express channelrhodopsin-2 (ChR2) in neuronal ensembles that were activated during contextual fear encoding in infant mice. We then asked whether reactivation of ChR2-tagged ensembles in the dentate gyrus was sufficient for memory recovery in adulthood. We found that optogenetic stimulation of tagged dentate gyrus neurons recovered "lost" infant memories up to 3 months following training and that memory recovery was associated with broader reactivation of tagged hippocampal and cortical neuronal ensembles.