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Nippon Ganka Gakkai Zasshi. 1996 Aug;100(8):575-81.

[Physiological roles of rhodopsin phosphorylation and dephosphorylation and its relationship with retinitis pigmentosa].

[Article in Japanese]

Author information

1
Department of Opthalmology, Sapporo Medical University School of Medicine, Hokkaido, Japan.

Abstract

Light signals are converted into electrical signals by vertebrate photoreceptor cells, and the generated electrical signals are then modulated within retinal neurons and brain. During the visual transduction precesses in the photoreceptor cells, there are basically three functions. That is, (1) photoexcitation, (2) quenching of the photoexcitation, and (3) adaptation. These functions are precisely regulated by enzymatic cascade reactions. Quite recently, it was shown that rhodopsin phosphorylation occurred at different sites with different kinetics, in vivo, and this may be a control mechanism for both quenching and adaptation. Furthermore, autosmal retinitis pigmentosa (RP) with rhodopsin mutation at 296 Lys, which in the binding site of 11-cis-retinal, showed constitutive activation of guanosine 5'-triphosphate (GTP) binding protein and no rhodopsin phosphorylation by rhodopsin kinase. These observations suggest that rhodopsin phosphorylation and dephosphorylation are critical for understanding visual transduction and pathophysiology of RP.

PMID:
8810231
[Indexed for MEDLINE]

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