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Calcium regulates the rate of rhodopsin disactivation and the primary amplification step in visual transduction.

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Wagner,  R.
Abteilung Neurobiologie, MPI for biophysical chemistry, Max Planck Society;

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Ryba,  N.
Department of Spectroscopy and Photochemical Kinetics, MPI for biophysical chemistry, Max Planck Society;

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Uhl,  R.
Abteilung Neurobiologie, MPI for biophysical chemistry, Max Planck Society;

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Citation

Wagner, R., Ryba, N., & Uhl, R. (1989). Calcium regulates the rate of rhodopsin disactivation and the primary amplification step in visual transduction. FEBS Letters, 242(2), 249-254. doi:10.1016/0014-5793(89)80479-X.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002C-640C-0
Abstract
The kinetics of the light-induced activation of transducin as well as the subsequent disactivation process can be monitored by means of a specific light scattering transient PA. In this communication it is demonstrated that the rate of transducin disactivation is calcium dependent, increasing when the calcium concentration is decreased. As a consequence of the accelerated recovery in low calcium, the time to the peak of the transducin activation process is shortened and the gain of the primary amplification step, i.e. the number of transducin molecules activated per bleached rhodopsin, is reduced. Experiments using hydroxylamine as an artificial quencher of rhodopsin activity suggest that calcium acts upon rhodopsin kinase and not upon the rate of the GTPase. This would indicate that calcium may control visual adaptation not only by regulating guanine cyclase activity, but also by affecting the primary step in the transduction cascade, the rhodopsin-transducin coupling