Abstract
In retinal rods, Ca(2+) exerts negative feedback control on cGMP synthesis by guanylate cyclase (GC). This feedback loop was disrupted in mouse rods lacking guanylate cyclase activating proteins GCAP1 and GCAP2 (GCAPs(-/-)). Comparison of the behavior of wild-type and GCAPs(-/-) rods allowed us to investigate the role of the feedback loop in normal rod function. We have found that regulation of GC is apparently the only Ca(2+) feedback loop operating during the single photon response. Analysis of the rods' light responses and cellular dark noise suggests that GC normally responds to light-driven changes in [Ca(2+)] rapidly and highly cooperatively. Rapid feedback to GC speeds the rod's temporal responsiveness and improves its signal-to-noise ratio by minimizing fluctuations in cGMP.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Artifacts
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Calcium / metabolism
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Calcium Signaling / physiology*
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Calcium-Binding Proteins / deficiency*
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Calcium-Binding Proteins / genetics
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Cyclic GMP / biosynthesis*
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Dark Adaptation / physiology
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Feedback / physiology*
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Guanylate Cyclase / metabolism*
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Guanylate Cyclase-Activating Proteins
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Hot Temperature
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Membrane Potentials / physiology
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Mice
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Mice, Knockout
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Photic Stimulation
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Photons
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Retinal Rod Photoreceptor Cells / cytology
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Retinal Rod Photoreceptor Cells / metabolism*
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Rhodopsin / metabolism
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Vision, Ocular / physiology
Substances
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Calcium-Binding Proteins
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Guanylate Cyclase-Activating Proteins
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Guca1a protein, mouse
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Guca1b protein, mouse
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Rhodopsin
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Guanylate Cyclase
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Cyclic GMP
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Calcium