Gold Paul E
Department of Psychology, Neuroscience Program, and Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Champaign, Illinois 61820, USA.
Learn Mem. 2006 Sep-Oct;13(5):506-14. doi: 10.1101/lm.277406.
Results from studies of retrograde amnesia provide much of the evidence for theories of memory consolidation. Retrograde amnesia gradients are often interpreted as revealing the time needed for the formation of long-term memories. The rapid forgetting observed after many amnestic treatments, including protein synthesis inhibitors, and the parallel decay seen in long-term potentiation experiments are presumed to reveal the duration of short-term memory processing. However, there is clear and consistent evidence that the time courses obtained in these amnesia experiments are highly variable within and across experiments and treatments. The evidence is inconsistent with identification of basic temporal properties of memory consolidation. Alternative views include modulation of memory and emphasize the roles that hormones and neurotransmitters have in regulating memory formation. Of related interest, converging lines of evidence suggest that inhibitors of protein synthesis and of other biochemical processes act on modulators of memory formation rather than on mechanisms of memory formation. Based on these findings, memory consolidation and reconsolidation studies might better be identified as memory modulation and "remodulation" studies. Beyond a missing and perhaps unattainable time constant of memory consolidation, some current views of memory consolidation assume that memories, once formed, are generally unmodifiable. It is this perspective that appears to have led to the recent interest in memory reconsolidation. But the view adopted here is that memories are continually malleable, being updated by new experiences and, at the same time, altering the memories of later experiences. Studies of memory remodulation offer promise of understanding the neurobiological bases by which new memories are altered by prior experiences and by which old memories are altered by new experiences.
逆行性遗忘的研究结果为记忆巩固理论提供了大量证据。逆行性遗忘梯度通常被解释为揭示了形成长期记忆所需的时间。在许多失忆治疗后观察到的快速遗忘,包括蛋白质合成抑制剂,以及在长时程增强实验中看到的平行衰退,被认为揭示了短期记忆处理的持续时间。然而,有明确且一致的证据表明,在这些失忆实验中获得的时间进程在实验和治疗内部及之间存在高度变异性。该证据与确定记忆巩固的基本时间特性不一致。其他观点包括记忆调制,并强调激素和神经递质在调节记忆形成中所起的作用。相关的有趣之处在于,越来越多的证据表明蛋白质合成和其他生化过程的抑制剂作用于记忆形成的调制因子而非记忆形成机制。基于这些发现,记忆巩固和再巩固研究或许更应被视为记忆调制和“再调制”研究。除了缺失且可能无法实现的记忆巩固时间常数外,当前一些关于记忆巩固的观点认为,记忆一旦形成通常就不可改变。正是这种观点似乎引发了近期对记忆再巩固的兴趣。但这里所采用的观点是,记忆是持续可塑的,会被新的经历更新,同时也会改变对后续经历的记忆。记忆再调制研究有望理解神经生物学基础,通过这些基础,新记忆会被先前经历改变,旧记忆会被新经历改变。