| Summary: | <p>Abstract</p> <p>Background</p> <p>GABAergic inhibition and effects of intracellular chloride ions on calcium channel activity have been proposed to regulate neurotransmission from photoreceptors. To assess the impact of these and other chloride-dependent mechanisms on release from cones, the chloride equilibrium potential (E<sub>Cl</sub>) was determined in red-sensitive, large single cones from the tiger salamander retinal slice.</p> <p>Results</p> <p>Whole cell recordings were done using gramicidin perforated patch techniques to maintain endogenous Cl<sup>- </sup>levels. Membrane potentials were corrected for liquid junction potentials. Cone resting potentials were found to average -46 mV. To measure E<sub>Cl</sub>, we applied long depolarizing steps to activate the calcium-activated chloride current (I<sub>Cl(Ca)</sub>) and then determined the reversal potential for the current component that was inhibited by the Cl<sup>- </sup>channel blocker, niflumic acid. With this method, E<sub>Cl </sub>was found to average -46 mV. In a complementary approach, we used a Cl-sensitive dye, MEQ, to measure the Cl<sup>- </sup>flux produced by depolarization with elevated concentrations of K<sup>+</sup>. The membrane potentials produced by the various high K<sup>+ </sup>solutions were measured in separate current clamp experiments. Consistent with electrophysiological experiments, MEQ fluorescence measurements indicated that E<sub>Cl </sub>was below -36 mV.</p> <p>Conclusions</p> <p>The results of this study indicate that E<sub>Cl </sub>is close to the dark resting potential. This will minimize the impact of chloride-dependent presynaptic mechanisms in cone terminals involving GABA<sub>a </sub>receptors, glutamate transporters and I<sub>Cl(Ca)</sub>.</p>
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