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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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 Creators:
Shih, Pei-Yu, Author
Savtchenko, Leonid P., Author
Kamasawa, Naomi1, Author
Dembitskaya, Yulia, Author
McHugh, Thomas J., Author
Rusakov, Dmitri A., Author
Shigemoto, Ryuichi, Author
Semyanov, Alexey, Author
Affiliations:
1Max Planck Florida Institute for Neuroscience, Max Planck Society, One Max Planck Way, Jupiter FL 33458, USA, ou_1950288              

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 Abstract: 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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 Dates: 2013-11-27
 Publication Status: Issued
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 Rev. Type: Peer
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Title: Cell Reports
Source Genre: Journal
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Pages: - Volume / Issue: 5 (4) Sequence Number: - Start / End Page: 941 - 951 Identifier: -