Sil'kis I G
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, Russia.
Neurosci Behav Physiol. 2010 Jan;40(1):5-19. doi: 10.1007/s11055-009-9230-7. Epub 2009 Dec 11.
Existing data on the involvement of the hippocampus in contextual memory and the fact that contextual memory is impaired in dreams occurring during paradoxical sleep allowed us to suggest that one of the causes of this impairment consists of changes in the efficiency of synaptic transmission in the hippocampus due to increases (as compared with waking) in the concentrations of acetylcholine, dopamine, and cortisol, as well as the absence of serotonin and noradrenaline. Our previous analysis showed that in paradoxical sleep, long-term depression can be induced all components of the polysynaptic pathway through the hippocampal formation, while potentiation can occur at the inputs from the entorhinal cortex to hippocampal fields CA1 and CA3 and in the associative connections in field CA3. It is hypothesized that the correct functioning of episodic memory requires efficient transmission of signals in each component of the polysynaptic pathway through the hippocampus, allowing a neuronal representation of the context to be created within it. In the state of waking, reproduction of the context of an episode simultaneously activates the neuronal representation of the context remembered in the hippocampus and neuronal representations of the details of the episode remembered in those areas of the cortex in which they were processed. It follows from the proposed mechanism that any neurotransmitter or neuropeptide able to promote longterm potentiation in all components of the polysynaptic pathway through the hippocampus can improve episodic memory. As the consequences of the mechanism are consistent with experimental data, it can be used to seek agents improving episodic memory.
关于海马体参与情境记忆的现有数据，以及快速眼动睡眠期间出现的梦境中情境记忆受损这一事实，使我们认为这种损伤的原因之一是，与清醒状态相比，乙酰胆碱、多巴胺和皮质醇浓度增加，同时血清素和去甲肾上腺素缺乏，导致海马体中突触传递效率发生变化。我们之前的分析表明，在快速眼动睡眠中，通过海马结构的多突触通路的所有成分都可诱导长时程抑制，而在内嗅皮质到海马CA1区和CA3区的输入以及CA3区的联合连接中可发生增强。据推测，情景记忆的正常运作需要通过海马体的多突触通路的每个成分有效传递信号，从而在其中创建情境的神经元表征。在清醒状态下，重现一个事件的情境会同时激活海马体中记住的情境的神经元表征，以及在处理这些事件细节的皮质区域中记住的事件细节的神经元表征。从所提出的机制可以推断，任何能够促进通过海马体的多突触通路的所有成分进行长时程增强的神经递质或神经肽都可以改善情景记忆。由于该机制的结果与实验数据一致，因此可用于寻找改善情景记忆的药物。
