Dendritic Mechanisms Controlling the Threshold and Timing Requirement of Synaptic Plasticity
Dendritic Mechanisms Controlling the Threshold and Timing Requirement of Synaptic Plasticity
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DOI：
10.1002/hipo.20748
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发表时间：
2011-03-01
期刊：
影响因子：
3.5
通讯作者：
Yuan, Li-Lian
中科院分区：
文献类型：
--
作者：
Zhao, Cuiping;Wang, Lang;Yuan, Li-Lian
位于神经元树突上并对其进行操作的主动电导有望调节突触整合和可塑性。我们研究了 Kv4.2 介导的 A 型 K+ 通道和 Ca2+ 激活的 K+ 通道如何参与需要相关突触前和突触后活动的赫布型可塑性的诱导过程。在 CA1 锥体神经元中，由 theta 爆发配对方案诱导的强大的长期增强 (LTP) 通常发生在一个狭窄的窗口内，在此期间传入的突触电位与突触后去极化同时发生。然而，消除 Kv4.2(-/-) 小鼠中树突 A 型 K+ 电流会导致时间窗口扩大，从而使突触增强的诱导不太依赖于突触前和突触后活动的时间关系。对于另一种类型的突触可塑性，即长期抑制，Kv4.2(-/-)小鼠的阈值显着增加。当诱导期间螯合适量的内部游离钙时，抑郁阈值的这种变化恢复到正常。与 A 型通道相配合，Ca2+ 激活的 K+ 通道也对突触可塑性产生滑动作用。在 Kv4.2(-/-) 小鼠中阻断这些通道会导致更大的增强，而相比之下，抑郁阈值进一步移动。总之，树突A型和Ca2+激活的K+通道以加性方式双重调节突触可塑性的时间依赖性和阈值。 (C) 2010 Wiley-Liss, Inc.
Active conductances located and operating on neuronal dendrites are expected to regulate synaptic integration and plasticity. We investigate how Kv4.2-mediated A-type K+ channels and Ca2+-activated K+ channels are involved in the induction process of Hebbian-type plasticity that requires correlated pre- and postsynaptic activities. In CA1 pyramidal neurons, robust long-term potentiation (LTP) induced by a theta burst pairing protocol usually occurred within a narrow window during which incoming synaptic potentials coincided with postsynaptic depolarization. Elimination of dendritic A-type K+ currents in Kv4.2(-/-) mice, however, resulted in an expanded time window, making the induction of synaptic potentiation less dependent on the temporal relation of pre- and postsynaptic activity. For the other type of synaptic plasticity, long-term depression, the threshold was significantly increased in Kv4.2(-/-) mice. This shift in depression threshold was restored to normal when the appropriate amount of internal free calcium was chelated during induction. In concert with A-type channels, Ca2+-activated K+ channels also exerted a sliding effect on synaptic plasticity. Blocking these channels in Kv4.2(-/-) mice resulted in an even larger potentiation while by contrast, the depression threshold was shifted further. In conclusion, dendritic A-type and Ca2+-activated K+ channels dually regulate the timing-dependence and thresholds of synaptic plasticity in an additive way. (C) 2010 Wiley-Liss, Inc.