The relative contribution of NMDARs to excitatory postsynaptic currents is controlled by Ca2+-induced inactivation
NMDA receptors (NMDARs) are important mediators of excitatory synaptic transmission and plasticity. A hallmark of these channels is their high permeability to Ca2+. At the same time, they are themselves inhibited by the elevation of intracellular Ca2+ concentration. It is unclear however, whether th...
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| Hauptverfasser: | , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
29 January 2016
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| In: |
Frontiers in cellular neuroscience
Year: 2016, Jahrgang: 10, Pages: 1-10 |
| ISSN: | 1662-5102 |
| DOI: | 10.3389/fncel.2016.00012 |
| Online-Zugang: | Verlag, kostenfrei, Volltext: https://doi.org/10.3389/fncel.2016.00012 Verlag, kostenfrei, Volltext: https://www.frontiersin.org/articles/10.3389/fncel.2016.00012/full 
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| Verfasserangaben: | Fliza Valiullina, Yulia Zakharova, Marat Mukhtarov, Andreas Draguhn, Nail Burnashev and Andrei Rozov |
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| 245 | 1 | 4 | |a The relative contribution of NMDARs to excitatory postsynaptic currents is controlled by Ca2+-induced inactivation |c Fliza Valiullina, Yulia Zakharova, Marat Mukhtarov, Andreas Draguhn, Nail Burnashev and Andrei Rozov |
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| 520 | |a NMDA receptors (NMDARs) are important mediators of excitatory synaptic transmission and plasticity. A hallmark of these channels is their high permeability to Ca2+. At the same time, they are themselves inhibited by the elevation of intracellular Ca2+ concentration. It is unclear however, whether the Ca2+ entry associated with single NMDAR mediated synaptic events is sufficient to self-inhibit their activation. Such auto-regulation would have important effects on the dynamics of synaptic excitation in several central networks. Therefore, we studied NMDAR-mediated synaptic currents in mouse hippocampal CA1 pyramidal neurons. Postsynaptic responses to subthreshold Schaffer collateral stimulation depended strongly on the absence or presence of intracellular Ca2+ buffers. Loading of pyramidal cells with exogenous Ca2+ buffers increased the amplitude and decay time of NMDAR mediated EPSCs (EPSP) and prolonged the time window for action potential generation. Our data indicate that the Ca2+ influx mediated by unitary synaptic events is sufficient to produce detectable self-inhibition of NMDARs even at a physiological Mg2+ concentration. Therefore, the contribution of NMDARs to synaptic excitation is strongly controlled by both previous synaptic activity as well as by the Ca2+ buffer capacity of postsynaptic neurons. | ||
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| 650 | 4 | |a Calcium | |
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| 650 | 4 | |a modulation | |
| 650 | 4 | |a NMDA receptor | |
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