Background: The rate-limiting step that determines the dominant time constant (τ(D)) of mammalian rod photoresponse recovery is the deactivation of the active phosphodiesterase (PDE6). Physiologically relevant Ca(2+)-dependent mechanisms that would affect the PDE inactivation have not been identified. However, recently it has been shown that τ(D) is modulated by background light in mouse rods.
Methodology/principal findings: We used ex vivo ERG technique to record pharmacologically isolated photoreceptor responses (fast PIII component). We show a novel static effect of calcium on mouse rod phototransduction: Ca(2+) shortens the dominant time constant (τ(D)) of saturated photoresponse recovery, i.e., when extracellular free Ca(2+) is decreased from 1 mM to ∼25 nM, the τ(D) is reversibly increased ∼1.5-2-fold.
Conclusions: We conclude that the increase in τ(D) during low Ca(2+) treatment is not due to increased [cGMP], increased [Na(+)] or decreased [ATP] in rod outer segment (ROS). Also it cannot be due to protein translocation mechanisms. We suggest that a Ca(2+)-dependent mechanism controls the life time of active PDE.