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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Animals, Calcium, Cyclic Nucleotide Phosphodiesterases, Type 6, In Vitro Techniques, Kinetics, Light, Light Signal Transduction, Mice, Mice, Inbred C57BL, Retina, Retinal Rod Photoreceptor Cells.
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Does calcium set the physiological value of the dominant time constant of saturated mouse rod photoresponse recovery? Context: 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. 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.
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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. Final Decision: yes