Nicoll
Lu, Gray, Granger, During, Nicoll • 2011 • J Neurophysiol - PDF
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We thus tested whether GluA2 is required for the potentiation of AMPAR EPSCs following the loss of NMDARs. In the GRIA2fl/fl mice, deleting GluA2 caused about a 50% reduction in the AMPAR EPSC (Fig. 3A ) with no change in the glutamate-evoked AMPAR-mediated outside-out patch currents (B ). Interestingly, in GRIA2fl/flGRIN1fl/fl mice the loss of NMDARs failed to enhance AMPAR EPSCs. In fact, there was a significant further decrease FIG: {{#info: 
{{{2}}} CLICK AWAY FROM IMAGE TO CLOSE }}. Neither genetic manipulation changes the PPR. In addition, as expected, deletion of GluA2 caused strong inward rectification. Finally, no difference was found in glutamate evoked AMPAR-mediated currents in outside-out patches FIG: {{#info: {{{2}}} CLICK AWAY FROM IMAGE TO CLOSE }}. Therefore in contrast to GluA1, the GluA2 subunit is critical for synaptic potentiation of AMPARs following NMDAR deletion.