FIGURE SUMMARY
Title

Cardiac Electrophysiological Effects of Light-Activated Chloride Channels

Authors
Kopton, R.A., Baillie, J.S., Rafferty, S.A., Moss, R., Zgierski-Johnston, C.M., Prykhozhij, S.V., Stoyek, M.R., Smith, F.M., Kohl, P., Quinn, T.A., Schneider-Warme, F.
Source
Full text @ Front. Physiol.

GtACR1 activation depolarizes ventricular myocyte membrane potential in isolated zebrafish hearts. Regions of high or no eGFP expression on the ventricle of 3-months post fertilization (mpf) zebrafish isolated hearts were illuminated by a 0.16 mm2 spot of 531/22 nm light sustained for 15 s or pulsed for 10 ms at a rate 2–3 × sinus heart rate. (A,D–E) In the case of sustained light, in regions displaying eGFP expression (red circle in C) there was an immediate increase in resting membrane potential (ER) and a decrease in the maximum rate of membrane depolarization (dE/dtmax), AP amplitude (APAmp), and APD at 50% and 90% repolarization (APD50 and APD90). (B) In the case of pulsed light, the heart could be stimulated when light intensity was increased to supra-threshold values. (A,B) In both cases, there was no effect seen in regions displaying no eGFP expression (blue circle in C). *indicates p < 0.0001 by two-tailed paired Student's t-test.

GtACR1 activation can inhibit ventricular myocyte action potentials in isolated zebrafish hearts. In a subset of 3-months post fertilization (mpf) isolated zebrafish hearts (n = 3/7), a 0.16 mm2 spot of 531/22 nm light applied to some eGFP expressing regions locally inhibited AP by depolarization of membrane potential, while there was no effect in regions with no eGFP expression (confirmed by live confocal microscopy).

Acknowledgments
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