FIGURE 5.
Chloride and salicylate dependence of specific membrane capacitance. ΔCsa is normalized by dividing by N (Qmax/ze) at 0 salicylate conditions. A, dashed lines show initial ΔCsa for each chloride condition in the absence of salicylate: upper panel, 140 mm chloride, 141 zF; middle panel, 20 mm chloride, 110 zF; lower panel, 10 mm chloride, 88 zF. Note that in each case ΔCsa is stable until a particular concentration of salicylate induces an increase in ΔCsa followed by a decrease. The onset of salicylate effects is chloride-dependent, arising at lower salicylate levels as chloride is reduced. The meno presto model, which incorporates prestin-dependent changes in Cm arising from changes in motor surface area/membrane thickness, follows this pattern. B, data from Homma and Dallos (15) (H. & D. 2011); see their supplemental Fig. S3A (140 mm [chlorine] internal). The dashed line shows an initial ΔCsa of 96 zF. A similar pattern of ΔCsa change is observed when salicylate concentration is changed. Both the salicylate Kd and the ΔCsa scaling factor for salicylate bound motors required adjustment to fit their data and are related to the higher salicylate sensitivity of mouse prestin (see “Results” for details). C, Clin also depends on the interaction between salicylate and chloride, showing a leftward shift along the salicylate concentration axis as chloride is reduced. The area motor model (gray lines) recapitulates this behavior. D, Homma and Dallos (15) Clin data are well described by the area motor model (see “Results”).