Nicoll
Journal Articles
Lu, Shi, Nicoll • 2009 • Cell - FullText
We found that approximately 80% of synaptic and >95% of somatic extrasynaptic receptors are GluA1A2 heteromers. The remaining receptors are GluA2A3 heteromers.
Our results, combined with previous work, indicate that GluA1 homomers—and indeed any AMPAR complex lacking GluA2—are excluded from the surface of CA1 pyramidal cells from animals at the age of 2–4 weeks under basal conditions.
The profound loss of functional synaptic AMPARs following the ablation of GluA1, coupled with the fact that the I/V of the synaptic currents remains linear, suggests that GluA2A3 receptors contribute 20% to basal synaptic transmission.
Since all surface AMPARs in CA1 pyramidal neurons contain GluA2, we were interested in how the cell responded to its loss. Following the transfection of Cre in slice cultures, the AMPAR EPSC amplitudes fell to 50% of control values at 6 days and then remained constant. rAAVCre-GFP experiments with GRIA2(fl/fl) mice also showed that loss of GluA2 caused a 50% loss of AMPAR EPSCs.
Is the decrease in the evoked synaptic responses due to a uniform loss of receptors across the entire population of synapses, as in the case with GluA1 deletion? To address this question, we examined mEPSCs. Remarkably, there was no change in the mean amplitude of mEPSCs but a dramatic reduction in frequency. This suggests that two processes occur during the loss of GluA2; approximately half of the synapses become devoid of AMPARs, while in the other half of synapses, GluA2-containing receptors are gradually replaced by GluA2-lacking receptors. This implies that there are two distinct populations of synapses, based on whether they can recruit GluA2-lacking receptors.
Granger, Shi, Lu, Nicoll • 2011 • Nature - FullText
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[[Category:Synaptic Plasticity]] [[Category:Journals]]
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