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. 3A ). 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. 3B ). Therefore in contrast to GluA1, the GluA2 subunit is critical for synaptic potentiation of AMPARs following NMDAR deletion.
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