Hardt Oliver, Wang Szu-Han, Nader Karim
Department of Psychology, McGill University, Montreal, Quebec, Canada.
Learn Mem. 2009 Mar 20;16(4):224-30. doi: 10.1101/lm.1267409. Print 2009 Apr.
To this day, it remains unresolved whether experimental amnesia reflects failed memory storage or the inability to retrieve otherwise intact memory. Methodological as well as conceptual reasons prevented deciding between these two alternatives: The absence of recovery from amnesia is typically taken as supporting storage impairment interpretations; however, this absence of recovery does not positively demonstrate nonexistence of memory, allowing for alternative interpretations of amnesia as impairment of memory retrieval. To address this shortcoming, we present a novel approach to study the nature of amnesia that makes positive, i.e., falsifiable, predictions for the absence of memory. Applying this paradigm, we demonstrate here that infusing anisomycin into the dorsal hippocampus induces amnesia by impairing memory storage, not retrieval.
时至今日,实验性失忆症究竟是反映了记忆存储失败还是无法检索原本完整的记忆,这一问题仍未得到解决。方法学以及概念上的原因使得无法在这两种可能性之间做出抉择:失忆症未出现恢复现象通常被视为支持存储损伤的解释;然而,这种未恢复现象并不能确凿地证明记忆不存在,这就使得失忆症可以被解释为记忆检索受损。为了解决这一缺陷,我们提出了一种研究失忆症本质的新方法,该方法对记忆缺失做出了肯定性的、即可证伪的预测。应用这一范式,我们在此证明,将茴香霉素注入背侧海马体会通过损害记忆存储而非检索来诱发失忆症。