Retrograde Synaptic Signaling Mediated by K+ Efflux through Postsynaptic NMDA 
Receptors

Shih, Pei-Yu; Savtchenko, Leonid P.; Kamasawa, Naomi; Dembitskaya, Yulia; McHugh, Thomas J.; Rusakov, Dmitri A.; Shigemoto, Ryuichi; Semyanov, Alexey

doi:10.1016/j.celrep.2013.10.026

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Retrograde Synaptic Signaling Mediated by K+ Efflux through Postsynaptic NMDA Receptors

Shih, P.-Y., Savtchenko, L., Kamasawa, N., Dembitskaya, Y., McHugh, T., Rusakov, D., et al. (2013). Retrograde Synaptic Signaling Mediated by K+ Efflux through Postsynaptic NMDA Receptors. Cell Reports, 5(4), 941-951. doi:10.1016/j.celrep.2013.10.026.

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Datensatz-Permalink: https://hdl.handle.net/11858/00-001M-0000-0019-0E27-F Versions-Permalink: https://hdl.handle.net/11858/00-001M-0000-0019-0E29-B

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Urheber:
Shih, Pei-Yu, Autor
Savtchenko, Leonid P., Autor
Kamasawa, Naomi¹, Autor
Dembitskaya, Yulia, Autor
McHugh, Thomas J., Autor
Rusakov, Dmitri A., Autor
Shigemoto, Ryuichi, Autor
Semyanov, Alexey, Autor

Affiliations:
1Max Planck Florida Institute for Neuroscience, Max Planck Society, One Max Planck Way, Jupiter FL 33458, USA, ou_1950288

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Zusammenfassung: 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.