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

First Author  Shih PY Year  2013
Journal  Cell Rep Volume  5
Issue  4 Pages  941-51
PubMed ID  24268779 Mgi Jnum  J:206845
Mgi Id  MGI:5553037 Doi  10.1016/j.celrep.2013.10.026
Citation  Shih PY, et al. (2013) Retrograde synaptic signaling mediated by K+ efflux through postsynaptic NMDA receptors. Cell Rep 5(4):941-51
abstractText  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.
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