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. 2016 Nov 17;6:37251. doi: 10.1038/srep37251

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Copyright © 2016, The Author(s)

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(A,B) Typical traces showing the action of GAS (300 μM) on C-eEPSCs in the absence (A) and presence of a nonselective antagonist of ASICs, amiloride (200 μM) (B). Quantitative summaries are plotted in (C,D) (n = 5, P < 0.05), respectively. (E) Representative traces showing that GAS-induced inhibition of spinal neuronal hyperexcitability in response to depolarizing current injection (F) and spontaneous firing in CFA-inflamed mice were significantly suppressed by the blockade of ASICs (n = 8, P < 0.05). (G) Quantitative analysis showing that GAS-induced inhibition of firing frequency (left) and GAS-induced increase of rheobase in CFA-inflamed mice was blocked by amiloride. (H) Quantitative analysis showing that GAS-induced inhibition of spontaneous firing was eliminated by amiloride. All data are represented as mean ± S.E.M. *P < 0.05.