Department of Systems Neuroscience, Cajal Institute-Consejo Superior de Investigaciones Científicas Madrid, Spain.
Front Neural Circuits. 2012 Oct 5;6:71. doi: 10.3389/fncir.2012.00071. eCollection 2012.
Long-term potentiation (LTP) is commonly used to study synaptic plasticity but the associated changes in the spontaneous activity of individual neurons or the computational properties of neural networks in vivo remain largely unclear. The multisynaptic origin of spontaneous spikes makes it difficult to estimate the impact of a particular potentiated input. Accordingly, we adopted an approach that isolates pathway-specific postsynaptic activity from raw local field potentials (LFPs) in the rat hippocampus in order to study the effects of LTP on ongoing spike transfer between cell pairs in the CA3-CA1 pathway. CA1 Schaffer-specific LFPs elicited by spontaneous clustered firing of CA3 pyramidal cells involved a regular succession of elementary micro-field-EPSPs (gamma-frequency) that fired spikes in CA1 units. LTP increased the amplitude but not the frequency of these ongoing excitatory quanta. Also, the proportion of Schaffer-driven spikes in both CA1 pyramidal cells and interneurons increased in a cell-specific manner only in previously connected CA3-CA1 cell pairs, i.e., when the CA3 pyramidal cell had shown pre-LTP significant correlation with firing of a CA1 unit and potentiated spike-triggered average (STA) of Schaffer LFPs following LTP. Moreover, LTP produced subtle reorganization of presynaptic CA3 cell assemblies. These findings show effective enhancement of pathway-specific ongoing activity which leads to increased spike transfer in potentiated segments of a network. They indicate that plastic phenomena induced by external protocols may intensify spontaneous information flow across specific channels as proposed in transsynaptic propagation of plasticity and synfire chain hypotheses that may be the substrate for different types of memory involving multiple brain structures.
长时程增强（LTP）通常用于研究突触可塑性，但个体神经元自发性活动或体内神经网络的计算特性的相关变化在很大程度上仍不清楚。自发尖峰的多突触起源使得很难估计特定增强输入的影响。因此，我们采用了一种方法，该方法可以将特定突触后的活性从大鼠海马体中的原始局部场电位（LFP）中分离出来，以便研究 LTP 对 CA3-CA1 通路中细胞对之间持续尖峰传递的影响。由 CA3 锥体神经元的自发簇状放电引起的 CA1 Schaffer 特异性 LFP 涉及到规则的基本微场-EPSP（伽马频率）序列，该序列在 CA1 单元中触发尖峰。LTP 增加了这些持续兴奋性量子的幅度，但不增加频率。此外，只有在先前连接的 CA3-CA1 细胞对中，Schaffer 驱动的尖峰在 CA1 锥体细胞和中间神经元中的比例才以细胞特异性的方式增加，即当 CA3 锥体细胞在 LTP 之前与 CA1 单元的发射显示出显著的相关性时，并增强了 LTP 后 Schaffer LFP 的尖峰触发平均（STA）。此外，LTP 导致了 CA3 细胞集合体的细微重构。这些发现表明，特定通路的持续活动得到了有效增强，从而导致网络中增强部分的尖峰传递增加。它们表明，外部协议诱导的塑性现象可能会增强特定通道中的自发信息流，正如在可塑性的突触间传播和 synfire 链假说中所提出的那样，这可能是涉及多个脑结构的不同类型记忆的基础。
