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

Fig. 3.

Fig. 3.

LPS-induced EPSC frequency increase involves purines acting on P2Y1. (A) TNF-α signaling is not involved in the microglial modulation of EPSC frequency, because the LPS response was not significantly different in slices from TNF-α (open circles) -deficient mice compared with WT mice (black circles). (B) The LPS-mediated EPSC frequency increase was blocked by broad spectrum purinergic antagonists RB-2 (n = 7) and PPADS (n = 7) and the P2Y1-specific antagonist MRS2179 (n = 5, mean ± SEM, t test, **P < 0.01). (C) Representative cumulative probability plots for IEI in the presence of MRS2179 before (black circles) and after (gray circles) LPS application. MRS2179 blocked the response to LPS in five of five recorded cells. (D) Representative cumulative probability plots for IEI before (black circles) and after (gray circles) MRS2365 application; seven of nine cells responded by an increased frequency in the presence of MRS2365 (KS test < 0.01). (E) The P2Y1 agonist MRS2365 (open circles) mimics the effect of LPS (black circles) on EPSC frequency (n = 9, mean ± SEM).