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Repeating or spacing learning sessions are strategies for memory improvement with shared molecular and neuronal components.
Neurobiology of Learning and Memory ( IF 2.7 ) Pub Date : 2020-05-01 , DOI: 10.1016/j.nlm.2020.107233
Verónica Cattaneo 1 , Alvaro San Martin 1 , Sergio E Lew 2 , Bruce D Gelb 3 , Mario R Pagani 1
Affiliation  

Intellectual disability is a common feature in genetic disorders with enhanced RAS-ERK1/2 signaling, including neurofibromatosis type 1 (NF1) and Noonan syndrome (NS). Additional training trials and additional spacing between trials, respectively, restores memory deficits in animal models of NF1 and NS. However, the relationship between the underlying mechanisms in these strategies remain obscure. Here, we developed an approach to examine the effect of adding training trials or spacing to a weak training protocol and used genetic and behavioral manipulations in Drosophila to explore such question. We found that repetition and spacing effects are highly related, being equally effective to improve memory in control flies and sharing mechanistic bases, including the requirement of RAS activity in mushroom body neurons and protein synthesis dependence. After spacing or repeating learning trials, memory improvement depends on the formation of long-term memory (LTM). Moreover, a disease-related gain-of-function RasV152G allele impaired LTM. Using minimal training protocols, we established that both learning strategies were also equally effective for memory rescue in the RasV152G mutant and showed non-additive interaction of the spacing and repetition effects. Memory improvement was never detected after Ras inhibition. We conclude that memory improvement by spacing or repeating training trials are two ways of using the same molecular resources, including RAS-ERK1/2-dependent signaling. This evidence supports the concept that learning problems in RAS-related disorders depend on the impaired ability to exploit the repetition and the spacing effect required for long-term memory induction.

中文翻译:

重复或间隔学习课程是利用共享的分子和神经元成分改善记忆的策略。

智力障碍是具有增强的RAS-ERK1 / 2信号传导的遗传性疾病的常见特征,包括1型神经纤维瘤病(NF1)和Noonan综合征(NS)。额外的训练试验和两次试验之间的额外间隔分别恢复了NF1和NS动物模型中的记忆缺陷。但是,这些策略中基本机制之间的关系仍然不清楚。在这里,我们开发了一种方法来检查在较弱的训练方案中增加训练试验或间隔的效果,并使用果蝇中的遗传和行为操作来探讨此类问题。我们发现重复和间隔效应是高度相关的,同等有效地提高了控制蝇的记忆并共享了机械基础,包括对蘑菇体神经元的RAS活性和蛋白质合成依赖性的要求。进行间隔或重复学习试验后,记忆力的改善取决于长期记忆力(LTM)的形成。此外,与疾病相关的功能获得性RasV152G等位基因损害LTM。使用最少的培训规程,我们确定两种学习策略在RasV152G突变体的记忆挽救中也同样有效,并且显示出间距和重复效应的非加性相互作用。抑制Ras后从未发现记忆改善。我们得出结论,通过间隔或重复训练试验来改善记忆是使用相同分子资源(包括RAS-ERK1 / 2依赖性信号传导)的两种方式。该证据支持这样的概念,即与RAS有关的疾病中的学习问题取决于长期记忆诱导所需的重复利用能力和间隔效应的削弱。
更新日期:2020-05-01
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