Sokolov M V, Rossokhin A V, Behnisch T, Reymann K G, Voronin L L
Brain Research Institute, Russian Academy of Medical Sciences, Moscow.
Neuroscience. 1998 Jul;85(1):1-13. doi: 10.1016/s0306-4522(97)00592-7.
Long-term potentiation is an experimental paradigm used to study synaptic plasticity and memory mechanisms. One similarity between long-term potentiation and memory is the existence of several distinct phases. However, our preliminary quantal analysis did not reveal essential differences in expression mechanisms of the early (< 1 h) and later (up to 3 h) phases of long-term potentiation. The data were compatible with presynaptic mechanisms of both phases. Another approach to distinguish between presynaptic and postsynaptic mechanisms is analysis of interaction between long-term potentiation and presynaptic paired-pulse facilitation. Such analysis had been previously done mainly with recordings of field potentials reflecting the activity of large neuronal populations. Only the early potentiation phase had been previously analysed with recordings from single neurons. The results from different groups were contradictory. In the present study, minimal excitatory postsynaptic potentials were recorded from CA1 pyramidal neurons of rat hippocampal slices. Paired-pulse facilitation ratios were calculated for various periods (up to 2-3 h) following induction of long-term potentiation. The ratio persistently decreased in the majority of neurons following long-term potentiation induction. The decrease in the paired-pulse facilitation ratio correlated with the magnitude of long-term potentiation and with the initial (pretetanic) facilitation ratio. Therefore, the general results of the present analysis was similar with the results of the quantal analysis: it is consistent with a strong involvement of presynaptic mechanisms in maintenance of both early and late phases of long-term potentiation. However, individual neurons could show variable changes in the paired-pulse facilitation, e.g., increases at late (> 0.5-1 h) periods after tetanus. Calculations of partial correlations and regression analysis indicated that positive correlation between potentiation magnitude and initial (pretetanic) paired-pulse facilitation tended to increase in the late potentiation phase (1.5-2.5 h post-tetanus) indicating that different mechanisms are involved in the early (0.5 h post-tetanus) and the late phase of long-term potentiation. The findings are compatible with involvement of presynaptic mechanisms in both the early and late phases of long-term potentiation. However, the results suggest that contribution of changes in release probability and in effective number of transmitter release sites may differ during the two phases. It is suggested that activation of silent synapses and increases in the number of transmission zones due to pre- and postsynaptic structural rearrangements represent important mechanisms of the late phase of long-term potentiation.
长时程增强是一种用于研究突触可塑性和记忆机制的实验范式。长时程增强与记忆之间的一个相似之处在于存在几个不同的阶段。然而，我们初步的量子分析并未揭示长时程增强早期（<1小时）和晚期（长达3小时）阶段表达机制的本质差异。这些数据与两个阶段的突触前机制相符。区分突触前和突触后机制的另一种方法是分析长时程增强与突触前配对脉冲易化之间的相互作用。此前这种分析主要是通过记录反映大量神经元群体活动的场电位来进行的。之前仅用单个神经元的记录对早期增强阶段进行过分析。不同研究小组的结果相互矛盾。在本研究中，从大鼠海马切片的CA1锥体神经元记录了最小兴奋性突触后电位。计算了长时程增强诱导后不同时间段（长达2 - 3小时）的配对脉冲易化比率。在大多数神经元中，长时程增强诱导后该比率持续下降。配对脉冲易化比率的下降与长时程增强的幅度以及初始（强直刺激前）易化比率相关。因此，本分析的总体结果与量子分析的结果相似：这与突触前机制在长时程增强早期和晚期维持中起重要作用是一致的。然而，单个神经元的配对脉冲易化可能会有不同变化，例如在强直刺激后晚期（>0.5 - 1小时）增加。偏相关计算和回归分析表明，增强幅度与初始（强直刺激前）配对脉冲易化之间的正相关在长时程增强晚期（强直刺激后1.5 - 2.5小时）趋于增加，这表明长时程增强早期（强直刺激后0.5小时）和晚期涉及不同机制。这些发现与突触前机制参与长时程增强早期和晚期过程相符。然而，结果表明在两个阶段中释放概率变化和递质释放位点有效数量变化的作用可能不同。有人提出，沉默突触的激活以及由于突触前和突触后结构重排导致的传递区域数量增加是长时程增强晚期的重要机制。
