According to the commonly accepted opinion, memory engrams are formed and stored at the level of neural networks due to a change in the strength of synaptic connections between neurons. This hypothesis of synaptic plasticity (HSP), formulated by Donald Hebb in the 1940s, continues to dominate the directions of experimental studies and the interpretations of experimental results in the field. The universal acceptance of the HSP has transformed it from a hypothesis into an incontrovertible theory. In this article, I show that the entire body of experimental and clinical data obtained in studies of long-term memory in mammals and humans is inconsistent with the HSP. Instead, these data suggest that long-term memory is formed and stored at the intracellular level where it is reliably protected from ongoing synaptic activity, including pathological epileptic activity. It seems that the generally accepted HSP became a serious obstacle to understanding the mechanisms of memory and that progress in this field requires rethinking this doctrine and shifting experimental efforts toward exploring the intracellular mechanisms.

根据普遍接受的观点，记忆印迹是由于神经元之间突触连接强度的变化而在神经网络层面形成和存储的。Donald Hebb 在 20 世纪 40 年代提出的突触可塑性 (HSP) 假说继续主导着该领域实验研究的方向和实验结果的解释。HSP 的普遍接受使其从假设转变为无可争议的理论。在本文中，我表明在哺乳动物和人类长期记忆研究中获得的全部实验和临床数据与 HSP 不一致。相反，这些数据表明，长期记忆是在细胞内水平形成和存储的，在细胞内水平上它受到可靠的保护，免受持续的突触活动（包括病理性癫痫活动）的影响。似乎普遍接受的 HSP 成为理解记忆机制的严重障碍，该领域的进展需要重新思考这一学说并将实验努力转向探索细胞内机制。