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首页> 外文期刊>Neuron >Regulation of dendritic excitability by activity-dependent trafficking of the A-type K+ channel subunit Kv4.2 in hippocampal neurons.
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Regulation of dendritic excitability by activity-dependent trafficking of the A-type K+ channel subunit Kv4.2 in hippocampal neurons.

机译：通过海马神经元中A型K +通道亚基Kv4.2的活动依赖性运输来调节树突状兴奋性。

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摘要

Voltage-gated A-type K+ channel Kv4.2 subunits are highly expressed in the dendrites of hippocampal CA1 neurons. However, little is known about the subcellular distribution and trafficking of Kv4.2-containing channels. Here we provide evidence for activity-dependent trafficking of Kv4.2 in hippocampal spines and dendrites. Live imaging and electrophysiological recordings showed that Kv4.2 internalization is induced rapidly upon glutamate receptor stimulation. Kv4.2 internalization was clathrin mediated and required NMDA receptor activation and Ca2+ influx. In dissociated hippocampal neurons, mEPSC amplitude depended on functional Kv4.2 expression level and was enhanced by stimuli that induced Kv4.2 internalization. Long-term potentiation (LTP) induced by brief glycine application resulted in synaptic insertion of GluR1-containing AMPA receptors along with Kv4.2 internalization. We also found evidence of Kv4.2 internalization upon synaptically evoked LTP in CA1 neurons of hippocampal slice cultures. These results present an additional mechanism for synaptic integration and plasticity through the activity-dependent regulation of Kv4.2 channel surface expression.
机译：电压门控A型K +通道Kv4.2亚基在海马CA1神经元的树突中高度表达。但是，对含Kv4.2的通道的亚细胞分布和运输知之甚少。在这里，我们为海马棘和树突中Kv4.2的活动依赖性运输提供了证据。实时成像和电生理记录表明，谷氨酸受体刺激后，Kv4.2内在化迅速被诱导。 Kv4.2内部化是网格蛋白介导的，需要NMDA受体激活和Ca2 +流入。在解离的海马神经元中，mEPSC振幅取决于功能性Kv4.2表达水平，并通过诱导Kv4.2内在化的刺激而增强。短暂应用甘氨酸诱导的长期增强（LTP）导致含有GluR1的AMPA受体的突触插入以及Kv4.2内在化。我们还发现海马切片培养的CA1神经元中突触诱发LTP后Kv4.2内在化的证据。这些结果提出了通过Kv4.2通道表面表达的活性依赖调节突触整合和可塑性的另一种机制。

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