Synaptic NMDA receptors (NMDARs) carry inward Ca2+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 Ca2+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.