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 gamma( PDE gamma) 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 gamma (T22A/T35A rods) adapt to light in a nearly normal manner. Because PDE gamma 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 alpha GTP. In PDE gamma T35A rods, a change in the conformation of the PDE gamma 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.
Modulation of phosphodiesterase6 turnoff during background illumination in mouse rod photoreceptors
Creators
Michael L. Woodruff - University of California, Los Angeles
Kerstin M. Janisch - Columbia University
Igor V. Peshenko - Salus University
Alexander M. Dizhoor - Salus University
Stephen H. Tsang - Columbia University
Gordon L. Fain - University of California, Los Angeles
Publication Details
The Journal of neuroscience, v 28(9), pp 2064-2074
Publisher
Soc Neuroscience
Number of pages
11
Grant note
R01 EY011522; EY01844; K08-EY004081; R37 EY001844; R01 EY001844-31; EY11522; R01 EY001844; R01 EY018213 / NEI NIH HHS; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Eye Institute (NEI)
Wellcome Trust; European Commission
R37EY001844 / NATIONAL EYE INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Eye Institute (NEI)
Resource Type
Journal article
Language
English
Academic Unit
Neurobiology and Anatomy; Pennsylvania College of Optometry (PCO)
Web of Science ID
WOS:000253549300009
Scopus ID
2-s2.0-39849089658
Other Identifier
991022035261504721
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