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首页> 外文期刊>Neuron >Rapid, bidirectional remodeling of synaptic NMDA receptor subunit composition by A-type K+ channel activity in hippocampal CA1 pyramidal neurons.
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Rapid, bidirectional remodeling of synaptic NMDA receptor subunit composition by A-type K+ channel activity in hippocampal CA1 pyramidal neurons.

机译：通过海马CA1锥体神经元的A型K +通道活性，快速，双向地重塑突触NMDA受体亚单位组成。

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摘要

The transient, A-type K+ current (IA) controls the excitability of CA1 pyramidal neuron dendrites by regulating the back-propagation of action potentials and by shaping synaptic input. Dendritic A-type K+ channels are targeted for modulation during long-term potentiation (LTP) and we have recently shown that activity-dependent internalization of the A-type channel subunit Kv4.2 enhances synaptic currents. However, the effect of changes in IA on the ability to induce subsequent synaptic plasticity (metaplasticity) has not been investigated. Here, we show that altering functional Kv4.2 expression level leads to a rapid, bidirectional remodeling of CA1 synapses. Neurons exhibiting enhanced IA showed a decrease in relative synaptic NR2B/NR2A subunit composition and did not exhibit LTP. Conversely, reducing IA by expression of a Kv4.2 dominant-negative or through genomic knockout of Kv4.2 led to an increased fraction of synaptic NR2B/NR2A and enhanced LTP. Bidirectional synaptic remodeling was mimicked in experiments manipulating intracellular Ca2+ and dependent on spontaneous activation of NMDA receptors and CaMKII activity. Our data suggest that A-type K+ channels are an integral part of a synaptic complex that regulates Ca2+ signaling through spontaneous NMDAR activation to control synaptic NMDAR expression and plasticity.
机译：瞬时的A型K +电流（IA）通过调节动作电位的反向传播和塑造突触输入来控制CA1锥体神经元树突的兴奋性。树突状A型K +通道的目标是在长期增强（LTP）期间进行调节，我们最近显示，A型通道亚基Kv4.2的依赖于活性的内在化增强了突触电流。但是，尚未研究IA变化对诱导随后的突触可塑性（间质可塑性）的影响。在这里，我们表明改变功能性Kv4.2表达水平导致CA1突触的快速，双向重塑。表现出增强的IA的神经元显示相对突触的NR2B / NR2A亚基组成减少，并且不表现出LTP。相反，通过表达Kv4.2显性负性或通过基因组敲除Kv4.2来减少IA导致突触NR2B / NR2A分数增加和LTP增强。在操纵细胞内Ca2 +的实验中模仿了双向突触重塑，并且依赖于NMDA受体的自发激活和CaMKII活性。我们的数据表明，A型K +通道是突触复合物的组成部分，该复合物通过自发NMDAR激活来调节Ca2 +信号传导，从而控制突触NMDAR的表达和可塑性。

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