Cell Reports
Volume 5, Issue 4, 27 November 2013, Pages 941-951
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Report
Retrograde Synaptic Signaling Mediated by K+ Efflux through Postsynaptic NMDA Receptors

https://doi.org/10.1016/j.celrep.2013.10.026Get rights and content
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Highlights

  • Postsynaptic NMDARs are the major source of synaptic K+ efflux

  • NMDAR-dependent K+ efflux is enhanced by coincidence of synaptic inputs

  • K+ elevation in the synaptic cleft enhances presynaptic Ca2+ transients

  • Retrograde K+ signaling is a form of computation in synaptic networks

Summary

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.

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Present address: Max Planck Florida Institute, Jupiter, FL 33458, USA