Latent memory facilitates relearning through molecular signaling mechanisms that are distinct from original learning.

Latent memory facilitates relearning through molecular signaling mechanisms that are distinct from original learning.
复制标题

潜在记忆通过与原始学习不同的分子信号机制促进重新学习。

DOI:
10.1016/j.nlm.2015.04.013
复制
发表时间:
2015
影响因子:
2.7
通讯作者:
Philips,GaryT
Philips,GaryT
中科院分区:
心理学4区
文献类型:
--
作者:
Menges,StevenA;Riepe,JoshuaR;Philips,GaryT

文献摘要

相似文献

记忆的一个高度保守的特征是,它可以以潜在的、非表达的状态存在,这在随后的学习过程中通过其显著促进(储存)或抑制(潜在抑制)随后的记忆形成的能力而被揭示。尽管潜在记忆无处不在,但潜在记忆痕迹的机械性质及其影响后续学习的能力仍然不清楚。模式生物加利福尼亚亚龙线虫提供了独特的机会,使行为和潜在的细胞和分子机制之间的强有力的联系。使用Ablasia,我们研究了由于潜在记忆而对先前被遗忘的经历进行储蓄的机制。我们先前报道了三种不同的记忆时间域的诱导节省:短期(10分钟),中期(2小时)和长期(24小时)。在这里,我们报告说,储蓄记忆的形成利用了与原始学习不同的分子信号传导途径:而幼稚动物原始中期和长期记忆的诱导需要有丝分裂原激活蛋白激酶(MAPK)激活和持续的蛋白质合成,2小时储蓄记忆不会受到MAPK或蛋白质合成抑制剂的干扰,24小时储蓄记忆不依赖于MAPK激活。总的来说,这些发现表明,在遗忘过程中,原始经验的潜在记忆可以通过与原始学习不同的分子信号机制促进再学习。
A highly conserved feature of memory is that it can exist in a latent, non-expressed state which is revealed during subsequent learning by its ability to significantly facilitate (savings) or inhibit (latent inhibition) subsequent memory formation. Despite the ubiquitous nature of latent memory, the mechanistic nature of the latent memory trace and its ability to influence subsequent learning remains unclear. The model organismAplysia californicaprovides the unique opportunity to make strong links between behavior and underlying cellular and molecular mechanisms. UsingAplysia, we have studied the mechanisms of savings due to latent memory for a prior, forgotten experience. We previously reported savings in the induction of three distinct temporal domains of memory: short-term (10 min), intermediate-term (2 h) and long-term (24 h). Here we report that savings memory formation utilizes molecular signaling pathways that are distinct from original learning: whereas the induction of both original intermediate- and long-term memory in naïve animals requires mitogen activated protein kinase (MAPK) activation and ongoing protein synthesis, 2 h savings memory is not disrupted by inhibitors of MAPK or protein synthesis, and 24 h savings memory is not dependent on MAPK activation. Collectively, these findings reveal that during forgetting, latent memory for the original experience can facilitate relearning through molecular signaling mechanisms that are distinct from original learning.