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Changes of the EPSP waveform regulate the temporal window for spike-timing-dependent plasticity

机译:EPSP波形的变化可调节时间窗口,从而获得与峰值定时相关的可塑性

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摘要

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. Copyright © 2007 Society for Neuroscience.
机译:使用包含与EPSP和突触后反向传播势能(BAP)配对的尖峰时序依赖性可塑性(STDP)协议,我们研究了慢Ca2 +依赖性K +介导的超极化(sAHP)诱导的EPSP波形变化的贡献)调节长时程增强(LTP)。通过减少EPSP的幅度和衰减时间常数,可以缩小诱导LTP所需的CA1锥体神经元中Schaffer侧支EPSP和BAP之间的>“时间窗口”,这可以用环噻嗪逆转。 EPSP的变化是由sAHP激活引起的电导增加引起的。因此,EPSP波形及其由sAHP进行的调节对于确定STDP的时间窗的持续时间至关重要,从而为认知过程的编码提供了可能的动态调节机制。版权所有©2007神经科学学会。

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