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首页> 外文期刊>Neuron >NMDA receptor subunit composition controls synaptic plasticity by regulating binding to CaMKII.
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NMDA receptor subunit composition controls synaptic plasticity by regulating binding to CaMKII.

机译：NMDA受体亚基组成通过调节与CaMKII的结合来控制突触可塑性。

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Calcium entry through postsynaptic NMDA-Rs and subsequent activation of CaMKII trigger synaptic plasticity in many brain regions. Active CaMKII can bind to NMDA-Rs, but the physiological role of this interaction is not well understood. Here, we test if association between active CaMKII and synaptic NMDA-Rs is required for synaptic plasticity. Switching synaptic NR2B-containing NMDA-Rs that bind CaMKII with high affinity with those containing NR2A, a subunit with low affinity for CaMKII, dramatically reduces LTP. Expression of NR2A with mutations that increase association to active CaMKII recovers LTP. Finally, driving into synapses NR2B with mutations that reduce association to active CaMKII prevents LTP. Spontaneous activity-driven potentiation shows similar results. We conclude that association between active CaMKII and NR2B is required for different forms of synaptic enhancement. The switch from NR2B to NR2A content in synaptic NMDA-Rs normally observed in many brain regions may contribute to reduced plasticity by controlling the binding of active CaMKII.
机译：钙通过突触后NMDA-Rs进入并随后激活CaMKII在许多脑区域触发突触可塑性。活跃的CaMKII可以与NMDA-Rs结合，但是这种相互作用的生理作用尚不十分清楚。在这里，我们测试活性CaMKII和突触NMDA Rs之间的关联是否需要突触可塑性。转换以高亲和力结合CaMKII的含有NR2B的突触的NMDA-R与含有NR2A（对CaMKII的亲和力低的亚基）的NMDA-R显着降低LTP。带有增加与活性CaMKII缔合的突变的NR2A表达可恢复LTP。最后，进入具有降低与活性CaMKII结合的突变的突触NR2B可防止LTP。自发活动驱动的增强显示类似的结果。我们得出结论，不同形式的突触增强需要活性CaMKII和NR2B之间的关联。通常在许多大脑区域中观察到的突触NMDA-R中，从NR2B含量向NR2A含量的转换可能通过控制活性CaMKII的结合而导致可塑性降低。

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