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Long-term memory consolidation or reconsolidation impairment induces amnesia with key characteristics that are similar to key learning characteristics.
Neuroscience & Biobehavioral Reviews ( IF 8.2 ) Pub Date : 2019-12-04 , DOI: 10.1016/j.neubiorev.2019.12.005
V P Nikitin 1 , S V Solntseva 1 , S A Kozyrev 1 , P V Nikitin 2
Affiliation  

According to a common perspective, amnesia is a passive consequence of memory consolidation or reconsolidation impairment. The results of our own study, as well as literature data, allowed us to offer an interpretation of amnesia. Amnesia is an active process whose key characteristics are similar to those of other long-term plastic rearrangements of the brain, including learning processes. In accordance with this hypothesis, the review considers the data we obtained on the mechanisms of amnesia induction and development caused by impairment of conditioned food aversion memory consolidation or reconsolidation. In particular, experimental data indicating the dependence of amnesia induction on protein and RNA syntheses are described. After amnesia induction, a time-dependent reorganization of its processes is shown to occur. In early amnesia stages (< 10 days), a gradual decrease in the possibility of memory formation during a second training was observed. In late stages of amnesia (10 days or more), an unusual physiological phenomenon was revealed-the second training did not lead to the formation of long-term memory. This effect was specific, as memory for a new type of food could possibly be formed in these animals. The described properties of amnesia facilitate its characterization as specific anterograde amnesia. In addition, at an early but not late amnesia stages, reminder presentation caused amnesia reactivation, impairment of which by DNA methyltransferase inhibitors caused memory recovery. The results obtained allow us to characterize amnesia as a specific, time-dependent, separate process. In conclusion, the potential biological significance of the described type of amnesia is considered, and we discuss the possible molecular mechanisms underlying it.

中文翻译:

长期记忆巩固或再整合障碍会导致健忘症,其关键特征与关键学习特征相似。

根据一个普遍的观点,健忘症是记忆整合或再整合损害的被动结果。我们自己的研究结果以及文献数据,使我们能够对健忘症进行解释。健忘症是一个活跃的过程,其关键特征与其他长期的大脑塑性重排(包括学习过程)相似。根据这一假设,本综述考虑了我们获得的有关条件性食物厌恶记忆巩固或再巩固损害引起的健忘症诱发和发育机制的数据。特别地,描述了指示失忆诱导对蛋白质和RNA合成的依赖性的实验数据。健忘症诱发后,其过程的时间依赖性重组得以发生。在早期健忘症阶段(<10天),在第二次训练中观察到记忆形成的可能性逐渐降低。在健忘症的晚期(10天或更长时间),发现了不寻常的生理现象-第二次训练并未导致长期记忆的形成。这种作用是特定的,因为在这些动物中可能会形成对新型食物的记忆。所描述的健忘症的特性有助于将其表征为特定的顺行性健忘症。此外,在早期但不是晚期的健忘症阶段,提醒提示会引起健忘症重新激活,而这种失忆是由于DNA甲基转移酶抑制剂引起的记忆恢复。获得的结果使我们能够将健忘症描述为一个特定的,与时间有关的独立过程。综上所述,
更新日期:2019-12-04
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