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Published Erratum
. 2017 Mar 28;114(13):E2799.
doi: 10.1073/pnas.1702629114. Epub 2017 Mar 6.

Correction for Hou et al., Homeostatic regulation of AMPA receptor expression at single hippocampal synapses

No authors listed
Published Erratum

Correction for Hou et al., Homeostatic regulation of AMPA receptor expression at single hippocampal synapses

No authors listed. Proc Natl Acad Sci U S A. .
No abstract available

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Figures

Fig. 5.
Fig. 5.
GluR2-lacking, calcium-permeable AMPARs are required for the induction of homeostatic response. (A) In neurons transfected with Syn-YFP and Kir2.1, homeostatic increase in GluR1 immunointensity (Upper) was completely blocked by coincubation with PhTx to specifically block the GluR2-lacking AMPARs (Lower). (B) Homeostatic response was blocked when PhTx was applied for only the first day or for 2 d after transfection. (Syn, 1.08 ± 0.06, n = 50; Kir2.1, 1.29 ± 0.08, n = 53; P < 0.05; Kir2.1 with PhTx-for 1 d, 1.09 ± 0.07, n = 61; P > 0.05; for 2 d 1.15 ± 0.06, n = 53; P > 0.05 compared with the Synapsin-YFP control). However, when supplemented only at the second day after transfection, PhTx failed to block the homeostatic response (1.24 ± 0.06, n = 56; P < 0.05 compared with Synapsin-YFP control), indicating a critical role of GluR2-lacking AMPARs in the early stages of homeostasis induction. (C) In neurons expressing Kir2.1 plus synapsin-YFP, 2-d incubation with PhTx did not change GluR1 intensity at normal synapses (n = 1,155). (D and E) TTX treatment (1 μM, 2 d) of cultured neurons induced global homeostatic increase in mEPSC amplitude (n = 15; P < 0.05). Coincubation of TTX (1 μM) and PhTx (5 μM) for 2 d abolished the TTX effect on mEPSC amplitude, indicating the critical role of GluR2-lacking AMPARs in homeostatic plasticity. A complete blockade of mEPSCs by CNQX confirmed AMPARs as the current mediators. (F) TTX-induced homeostatic increase in mEPSC amplitude was blocked by Naspm (n = 5).
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