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The Journal of Neuroscience, February 27, 2008, 28(9):2064-2074; doi:10.1523/JNEUROSCI.2973-07.2008

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Cellular/Molecular
Modulation of Phosphodiesterase6 Turnoff during Background Illumination in Mouse Rod Photoreceptors

Michael L. Woodruff,¹ Kerstin M. Janisch,² Igor V. Peshenko,³ Alexander M. Dizhoor,³ Stephen H. Tsang,² and Gordon L. Fain^1,4

¹Department of Physiological Science, University of California Los Angeles, Los Angeles, California 90095-1606, ²Brown Glaucoma Laboratory, Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, ³Hafter Research Laboratories, Pennsylvania College of Optometry, Elkins Park, Pennsylvania 19027, and ⁴Jules Stein Eye Institute, University of California Los Angeles School of Medicine, Los Angeles, California 90095-7000

Correspondence should be addressed to Prof. Gordon L. Fain, Department of Physiological Science, University of California Los Angeles, 3836 Life Sciences, Los Angeles, CA 90095-1606. Email: gfain{at}ucla.edu

In rod photoreceptors of wild-type mice, background light produces an acceleration of the decay of responses to brief flashes, accompanied by a decrease in the rate-limiting time constant for response decay. In rods in which phosphodiesterase (PDE) lacks one of its sites of phosphorylation (T35A rods), both the waveform of response decay and the rate-limiting time constant are nearly unaffected by backgrounds. These effects are not the result of the removal of the phosphorylation site per se, because rods lacking both of the phosphorylation sites of PDE (T22A/T35A rods) adapt to light in a nearly normal manner. Because PDE is one of the proteins of the GTPase activating protein (GAP) complex, our experiments argue for a novel mechanism of photoreceptor light adaptation produced by modulation of GAP-dependent hydrolysis of transducin GTP. In PDE T35A rods, a change in the conformation of the PDE subunit may hinder or mask this mechanism, which in mammals appears to be primarily responsible for the quickening of the temporal resolution of the rod response in backgrounds. Modulation of PDE turnoff also helps to prevent premature saturation of the rod in bright backgrounds, thus making an important contribution to light adaptation. Our experiments provide evidence for modulation of GAP protein-dependent response turnoff, which may also play a role in controlling signal duration at hormone receptors and synapses in the CNS.

Key words: photoreceptor; rod; transduction; adaptation; phosphodiesterase; vision

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Received June 29, 2007; revised Dec. 12, 2007; accepted Jan. 7, 2008.

Correspondence should be addressed to Prof. Gordon L. Fain, Department of Physiological Science, University of California Los Angeles, 3836 Life Sciences, Los Angeles, CA 90095-1606. Email: gfain{at}ucla.edu

This article has been cited by other articles:

				Y. Zhang, L. L. Molday, R. S. Molday, S. S. Sarfare, M. L. Woodruff, G. L. Fain, T. W. Kraft, and S. J. Pittler Knockout of GARPs and the {beta}-subunit of the rod cGMP-gated channel disrupts disk morphogenesis and rod outer segment structural integrity J. Cell Sci., April 15, 2009; 122(8): 1192 - 1200. [Abstract] [Full Text] [PDF]

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