Department of Psychology, McGill University, Montreal, Quebec H3A 1B1, Canada; email:
Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec H3A 2B4, Canada.
Annu Rev Neurosci. 2020 Jul 8;43:297-314. doi: 10.1146/annurev-neuro-091319-024636. Epub 2020 Feb 25.
An enduring problem in neuroscience is determining whether cases of amnesia result from eradication of the memory trace (storage impairment) or if the trace is present but inaccessible (retrieval impairment). The most direct approach to resolving this question is to quantify changes in the brain mechanisms of long-term memory (BM-LTM). This approach argues that if the amnesia is due to a retrieval failure, BM-LTM should remain at levels comparable to trained, unimpaired animals. Conversely, if memories are erased, BM-LTM should be reduced to resemble untrained levels. Here we review the use of BM-LTM in a number of studies that induced amnesia by targeting memory maintenance or reconsolidation. The literature strongly suggests that such amnesia is due to storage rather than retrieval impairments. We also describe the shortcomings of the purely behavioral protocol that purports to show recovery from amnesia as a method of understanding the nature of amnesia.
神经科学中一个持久的问题是确定遗忘症病例是源于记忆痕迹的消除(存储损伤),还是记忆痕迹存在但无法访问(检索损伤)。解决这个问题最直接的方法是量化长期记忆脑机制(BM-LTM)的变化。这种方法认为,如果遗忘症是由于检索失败引起的,那么 BM-LTM 应该保持在与受过训练、未受损的动物相当的水平。相反,如果记忆被抹去,BM-LTM 应该降低到类似于未受过训练的水平。在这里,我们回顾了一些通过针对记忆维持或再巩固来诱导遗忘症的研究中使用 BM-LTM 的情况。文献强烈表明,这种遗忘症是由于存储而不是检索损伤引起的。我们还描述了纯粹的行为协议的缺点,该协议声称作为理解遗忘症性质的一种方法,可以从遗忘症中恢复过来。