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. 2017 May 9;4(2):ENEURO.0105-17.2017. doi: 10.1523/ENEURO.0105-17.2017

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Copyright © 2017 Patel et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 8. — Increase in the cell-surface levels of GluA1 and GluA2 subunits of AMPARs in TMEV-infected TNFR2^–/– mice during acute seizures. (A) Representative immunoblots from two mice show the levels of GluA1 in the total as well as the cell-surface fractions of proteins isolated from ipsilateral hippocampus at 5 d postinjection of PBS (control) or TMEV. The surface proteins were isolated by cell-surface biotinylation procedure in acute hippocampal slices. Levels of GluA1 were quantified by densitometry, and data are shown as ratio of surface to total protein that is significantly increased in TMEV-infected mice (n = 6). PAG is a mitochondrial protein and serves as an intracellular control protein. (B) Similar to GluA1, the ratio of surface/total level for GluA2 is also increased in TMEV-infected mice (n = 6). (C) Ratios of surface/total protein expression for GluA1 and GluA2 are increased by 44% and 34%, respectively (data normalized to control). (D) Approximately 50% decrease in the total expression of GluA1 and GluA2 in TMEV-infected mice compared with control group. Statistics: unpaired two-tailed t test.