RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan.
UCL Institute of Neurology, University College London, London WC1N 3BG, UK.
Cell Rep. 2013 Nov 27;5(4):941-51. doi: 10.1016/j.celrep.2013.10.026. Epub 2013 Nov 21.
Synaptic NMDA receptors (NMDARs) carry inward Ca(2+) current responsible for postsynaptic signaling and plasticity in dendritic spines. Whether the concurrent K(+) efflux through the same receptors into the synaptic cleft has a physiological role is not known. Here, we report that NMDAR-dependent K(+) efflux can provide a retrograde signal in the synapse. In hippocampal CA3-CA1 synapses, the bulk of astrocytic K(+) current triggered by synaptic activity reflected K(+) efflux through local postsynaptic NMDARs. The local extracellular K(+) rise produced by activation of postsynaptic NMDARs boosted action potential-evoked presynaptic Ca(2+) transients and neurotransmitter release from Schaffer collaterals. Our findings indicate that postsynaptic NMDAR-mediated K(+) efflux contributes to use-dependent synaptic facilitation, thus revealing a fundamental form of retrograde synaptic signaling.
突触 NMDA 受体（NMDAR）携带内向 Ca（2+）电流，负责树突棘中的突触后信号传递和可塑性。目前尚不清楚通过相同受体进入突触间隙的同时 K（+）外流是否具有生理作用。在这里，我们报告说，NMDAR 依赖性的 K（+）外流可以在突触中提供逆行信号。在海马 CA3-CA1 突触中，由突触活动触发的大部分星形胶质细胞 K（+）电流反映了通过局部突触后 NMDAR 的 K（+）外流。激活突触后 NMDAR 产生的局部细胞外 K（+）升高增强了动作电位诱发的突触前 Ca（2+）瞬变和来自 Schaffer 侧枝的神经递质释放。我们的发现表明，突触后 NMDAR 介导的 K（+）外流有助于依赖使用的突触易化，从而揭示了一种基本的逆行突触信号传递形式。
