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Figure 1. PIP3 or PIP2 potentiates relative cAMP efficacy for homomeric CNGA3 channels. (A) Representative current traces for homomeric CNGA3 channels, elicited by saturating concentrations of cGMP (1 mM, green) or cAMP (10 mM, red), before and after 1 µM PIP3 (diC8-PIP3) application, and after subsequent application of 25 µg/ml poly-lysine (poly-K). Currents were elicited by voltage steps from a holding potential of 0 mV to +80 mV, then to −80 mV and 0 mV (inset). Leak currents in the absence of cyclic nucleotide were subtracted. The arrowhead indicates Imax elicited by cAMP in the presence of PIP3. (B) Time course for the change in maximal cAMP current (in 10 mM cAMP) induced by 1 µM PIP3; also shown is reversal by 25 µg/ml poly-K. Horizontal bars indicate application of respective agents; currents were not recorded during poly-K application. (C) Summary illustrating PIP3 (diC8-PIP3)- or PIP2 (diC8-PIP2)-dependent changes in Imax cAMP/cGMP for CNGA3 and CNGA1 homomeric channels (normalized to control values before treatment). Data are from 10–12 (for PIP3) or 3–4 (for PIP2) independent experiments; *, P < 0.05 relative to before PIPn application (control). The broken horizontal line refers to normalization to the value for Imax cAMP/cGMP of control patches. Error bars indicate mean ± SEM. Image published in: Dai G et al. (2013) © 2013 Dai et al. This image is reproduced with permission of the journal and the copyright holder. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike license Larger Image Printer Friendly View

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