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. 2011 Dec 13;109(4):E197–E205. doi: 10.1073/pnas.1111098109

Fig. 2.

Fig. 2.

LPS-induced EPSC frequency increase is mediated by the TLR4 pathway and requires microglia. (A) Triple immunostainings showing the expression of Iba1 (red in Right), a microglial marker, GFAP (green in Right), an astrocyte marker, and NeuN (blue in Right), a neuronal marker in organotypic slices from WT (Upper) or Pu-1−/− mice (Lower). (Scale bar: 50 μm.) (B, Left) Histogram representing the change in EPSC frequency on LPS application on WT acute slices (n = 12) and WT organotypic slices (n = 8) and the absence of response in Pu-1 (n = 9) organotypic slice culture (mean ± SEM, t test, **P < 0.01). (B, Right) Corresponding representative cumulative probability plots for IEI before (black circles) and after (gray circles) application of LPS in WT (Upper Right) and Pu1−/− (Lower Right). In WT slices, seven of nine cells responded to LPS (KS test; P < 0.01). Histogram in C Left shows that the response to LPS is blocked by minocycline and absent in slices from mice lacking TLR4 (TLR4−/−; mean ± SEM, t test, **P < 0.01). (C Right) Corresponding representative probability plots for IEI before (black circles) and after (gray circles) application of LPS in the presence of minocyclin (Upper Right) and TLR4−/− (Lower Right).