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  Indian J Med Microbiol
 

Figure 7: (A) Representative traces for IhERG1a (Ai) iherg1a/1b (Aii) and IhERG1b (Aiii) before and during exposure to 3 μM fluoxetine at room temperature. Lower panels show voltage protocols used. (B) Concentration-response relationships. At room temperature, fluoxetine inhibited 1a (open circles) with an IC50of 1.87 μM (confidence interval 1.48–2.37 μM). hERG 1a/1b (triangles) and hERG 1b (squares) dose–response relationships showed similar IC50values (n = 4–7 cells per concentration) and were inhibited, respectively, with an IC50of 3.02 μM (confidence interval 2.20–4.14 μM) (P > 0.05 vs. 1a) and an IC50of 3.31 μM (confidence interval 2.55–4.35 μM) (P > 0.05 vs. 1a)

Figure 7: (A) Representative traces for I<sub>hERG1a</sub> (Ai) i<sub>herg1a/1b</sub> (Aii) and I<sub>hERG1b</sub> (Aiii) before and during exposure to 3 μM fluoxetine at room temperature. Lower panels show voltage protocols used. (B) Concentration-response relationships. At room temperature, fluoxetine inhibited 1a (open circles) with an IC<sub>50</sub>of 1.87 μM (confidence interval 1.48–2.37 μM). hERG 1a/1b (triangles) and hERG 1b (squares) dose–response relationships showed similar IC<sub>50</sub>values (<i>n</i> = 4–7 cells per concentration) and were inhibited, respectively, with an IC<sub>50</sub>of 3.02 μM (confidence interval 2.20–4.14 μM) (<i>P</i> > 0.05 vs. 1a) and an IC<sub>50</sub>of 3.31 μM (confidence interval 2.55–4.35 μM) (<i>P</i> > 0.05 vs. 1a)