The relative contribution of NMDARs to excitatory postsynaptic currents is controlled by Ca2+-induced inactivation

• Verfasst von: Valiullina, Fliza [VerfasserIn]
• Verfasst von: Zakharova, Yulia [VerfasserIn]
• Verfasst von: Mukhtarov, Marat [VerfasserIn]
• Verfasst von: Draguhn, Andreas [VerfasserIn]
• Verfasst von: Burnashev, Nail [VerfasserIn]
• Verfasst von: Rozov, Andrei [VerfasserIn]
• Titel: The relative contribution of NMDARs to excitatory postsynaptic currents is controlled by Ca2+-induced inactivation
• Verf.angabe: Fliza Valiullina, Yulia Zakharova, Marat Mukhtarov, Andreas Draguhn, Nail Burnashev and Andrei Rozov
• E-Jahr: 2016
• Jahr: 29 January 2016
• Umfang: 10 S.
• Illustrationen: Diagramme
• Fussnoten: 2+ im Titel ist hochgestellt ; Gesehen am 29.05.2020
• Titel Quelle: Enthalten in: Frontiers in cellular neuroscience
• Ort Quelle: Lausanne : Frontiers Research Foundation, 2007
• Jahr Quelle: 2016
• Band/Heft Quelle: 10(2016) vom: Jan., Artikel-ID 12, Seite 1-10
• ISSN Quelle: 1662-5102
• DOI: doi:10.3389/fncel.2016.00012
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Action Potentials
• Sach-SW: Calcium
• Sach-SW: excitation
• Sach-SW: firing properties
• Sach-SW: modulation
• Sach-SW: NMDA receptor
• K10plus-PPN: 1699061637

Abstract

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.