Format

Send to

Choose Destination
Cell Rep. 2013 Nov 27;5(4):941-51. doi: 10.1016/j.celrep.2013.10.026. Epub 2013 Nov 21.

Retrograde synaptic signaling mediated by K+ efflux through postsynaptic NMDA receptors.

Author information

1
RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan.
2
UCL Institute of Neurology, University College London, London WC1N 3BG, UK.
3
National Institute for Physiological Sciences, Myodaiji, Okazaki 444-8787, Japan.
4
RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan; University of Nizhny Novgorod, Nizhny Novgorod 603950, Russia.
5
RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan; University of Nizhny Novgorod, Nizhny Novgorod 603950, Russia. Electronic address: semyanov@brain.riken.jp.

Abstract

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.

PMID:
24268779
DOI:
10.1016/j.celrep.2013.10.026
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center