The effects of ion channel blockers and ion substitutions on the prolonged depolarization of cones in the retina of the turtle (Pseudemys scripta elegans) were studied by intracellular recording. The results of current injection experiments indicate that the prolonged depolarization is regenerative and accompanied by a reduction in the cone's input resistance. The addition of cobalt (5-10 mM) or the removal of extracellular calcium suppressed the prolonged depolarization. Raising extracellular calcium or adding strontium (10 mM) lowered the threshold and increased the duration of the response. Unlike the feedback spikes of turtle cones studied by Piccolino and Gerschenfeld, the prolonged depolarization was not blocked by the organic calcium channel blocker, D600. Adding a calcium chelator, ethylene glycol-bis(β-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), to the electrolyte caused a progressive shortening of the prolonged depolarization until it was ultimately abolished. Lowering extracellular sodium or use of the potassium channel blockers tetraethylammonium (TEA) and 4-aminopyridine (4-AP) had little effect on the prolonged depolarization. Removing chloride from the superfusate induced a significant enhancement of the prolonged depolarization. In normal superfusate, the response tended to be of larger amplitude when recorded with electrodes containing chloride [1.5 M KCl + 1.5 M potassium acetate (KA)] rather than KA or potassium methylsulfate (KM) alone. The results suggest that the prolonged depolarization is initiated by the regenerative activation of voltage-sensitive calcium channels and sustained by a calcium-dependent chloride efflux. The present findings are also discussed in relation to the functional significance of the prolonged depolarization and mechanisms for the surround antagonism of cones in situ.
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