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首页> 外文期刊>eLife journal >Dendritic small conductance calcium-activated potassium channels activated by action potentials suppress EPSPs and gate spike-timing dependent synaptic plasticity
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Dendritic small conductance calcium-activated potassium channels activated by action potentials suppress EPSPs and gate spike-timing dependent synaptic plasticity

机译:动作电位激活的树突状小电导钙激活钾通道抑制EPSPs和门尖峰时序依赖的突触可塑性

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Small conductance calcium-activated potassium channels (SK channels) are present in spines and can be activated by backpropagating action potentials (APs). This suggests they may play a critical role in spike-timing dependent synaptic plasticity (STDP). Consistent with this idea, EPSPs in both cortical and hippocampal pyramidal neurons were suppressed by preceding APs in an SK-dependent manner. In cortical pyramidal neurons EPSP suppression by preceding APs depended on their precise timing as well as the distance of activated synapses from the soma, was dendritic in origin, and involved SK-dependent suppression of NMDA receptor activation. As a result SK channel activation by backpropagating APs gated STDP induction during low-frequency AP-EPSP pairing, with both LTP and LTD absent under control conditions but present after SK channel block. These findings indicate that activation of SK channels in spines by backpropagating APs plays a key role in regulating both EPSP amplitude and STDP induction.
机译:小电导的钙激活钾通道(SK通道)存在于棘中,并且可以通过反向传播的动作电位(AP)来激活。这表明它们可能在依赖尖峰时间的突触可塑性(STDP)中发挥关键作用。与这个想法一致,皮质和海马锥体神经元中的EPSPs被先前的AP以SK依赖的方式抑制。在皮层锥体神经元中,先前的AP抑制EPSP取决于它们的精确时机以及激活的突触与躯体的距离,起源于树突状,并涉及SK依赖性的NMDA受体激活的抑制。结果,在低频AP-EPSP配对过程中,通过反向传播AP进行门控STDP感应的SK通道激活,在控制条件下LTP和LTD均不存在,但出现在SK通道阻滞之后。这些发现表明,通过反向传播的AP激活棘突中的SK通道在调节EPSP振幅和STDP诱导中起关键作用。

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