%0 Journal Article
%A Prius Mengual, José
%A Pérez Rodríguez, Mikel
%A Andrade Talavera, Yuniesky
%A Rodríguez-Moreno, Antonio
%T NMDA Receptors containing GluN2B/2C/2D subunits mediate an increase in glutamate release at hippocampal CA3-CA1 synapses
%D 2019
%U https://hdl.handle.net/10433/23705
%X NMDA receptors (NMDARs) are involved in synaptic transmission and synaptic plasticity in different brain regions, and they modulate glutamate release at different presynaptic sites. Here, we studied whether non-postsynaptic NMDARs, putatively presynaptic (preNMDARs), are tonically active at hippocampal CA3-CA1 synapses, and if they modulate glutamate release. We found that when postsynaptic NMDARs are blocked by MK801, D-AP5 depresses evoked and spontaneous excitatory synaptic transmission, indicating that preNMDARs are tonically active at CA3-CA1 synapses, facilitating glutamate release. The subunit composition of these NMDARs was determined by studying evoked and spontaneous excitatory synaptic transmission in the presence of Zn2+, Ro 25-6981, and PPDA, antagonists of NMDARs containing GluN2A, GluN2B, and GluN2C/D, respectively. We found that evoked and spontaneous release decreased when the activity of NMDARs containing GluN2B and GluN2C/D subunits but not GluN2A was impeded. In addition, we found that the increase in glutamate release mediated by these NMDARs requires protein kinase A (PKA) activation. We conclude that preNMDARs that contain GluN2B and GluN2C/2D subunits facilitate glutamate release at hippocampal CA3-CA1 synapses through a mechanism that involves PKA.
%K Glutamate release
%K NMDA receptor
%K Presynaptic
%K Protein kinase A
%K Subunit composition
%K Tonic activation
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