Memory: Synaptic or Cellular, That Is the Question

Abstract

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.

Advancements in the study of synaptic plasticity and mitochondrial autophagy relationship

“…Stable synaptic connections ensure the reliable transmission of information between neurons, thus maintaining the normal functioning of the nervous system. In contrast, unstable synaptic connections can lead to unreliable and disrupted information transmission, thereby affecting the normal functioning of the nervous system (Arshavsky, 2023;Sadigh-Eteghad et al, 2018). Mitochondria, vital organelles within cells, serve as the cellular powerhouses responsible for energy metabolism.…”