兴奋性突触后电位（EPSP）波形的变化调节了依赖于峰电位时间的可塑性的时间窗口。
Changes of the EPSP waveform regulate the temporal window for spike-timing-dependent plasticity.
作者信息
Fuenzalida Marco, Fernandez de Sevilla David, Buño Washington
机构信息
Instituto Cajal, Consejo Superior de Investigaciones Científicas, 28002 Madrid, Spain.
出版信息
J Neurosci. 2007 Oct 31;27(44):11940-8. doi: 10.1523/JNEUROSCI.0900-07.2007.
Abstract
Using spike-timing-dependent plasticity (STDP) protocols that consist of pairing an EPSP and a postsynaptic backpropagating action potential (BAP), we investigated the contribution of the changes in EPSP waveform induced by the slow Ca2+-dependent K+-mediated afterhyperpolarization (sAHP) in the regulation of long-term potentiation (LTP). The "temporal window" between Schaffer collateral EPSPs and BAPs in CA1 pyramidal neurons required to induce LTP was narrowed by a reduction of the amplitude and decay time constant of the EPSP, which could be reversed with cyclothiazide. The EPSP changes were caused by the increased conductance induced by activation of the sAHP. Therefore, the EPSP waveform and its regulation by the sAHP are central in determining the duration of the temporal window for STDP, thus providing a possible dynamic regulatory mechanism for the encoding of cognitive processes.
摘要
我们使用由兴奋性突触后电位（EPSP）与突触后反向传播动作电位（BAP）配对组成的依赖于峰电位时间的可塑性（STDP）协议，研究了由缓慢的钙依赖性钾介导的超极化后电位（sAHP）诱导的EPSP波形变化在长时程增强（LTP）调节中的作用。诱导LTP所需的CA1锥体神经元中沙费尔侧支EPSP与BAP之间的“时间窗口”因EPSP幅度和衰减时间常数的降低而变窄，而环噻嗪可使其逆转。EPSP的变化是由sAHP激活诱导的电导增加引起的。因此，EPSP波形及其由sAHP的调节在确定STDP时间窗口的持续时间中起核心作用，从而为认知过程的编码提供了一种可能的动态调节机制。
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