Characterisation of dark adaptation in human cone pathways: an applicationof the equivalent background hypothesis

Citation
Mj. Pianta et M. Kalloniatis, Characterisation of dark adaptation in human cone pathways: an applicationof the equivalent background hypothesis, J PHYSL LON, 528(3), 2000, pp. 591-608
Citations number
51
Categorie Soggetti
Physiology
Journal title
JOURNAL OF PHYSIOLOGY-LONDON
ISSN journal
00223751 → ACNP
Volume
528
Issue
3
Year of publication
2000
Pages
591 - 608
Database
ISI
SICI code
0022-3751(20001101)528:3<591:CODAIH>2.0.ZU;2-O
Abstract
1. It is well accepted that in rod photoreceptors the photoproducts generat ed by a bleach cause desensitisation during dark adaptation. We examine whe ther this notion holds for cones. 2. A model of cone dark adaptation is developed based on the equivalent bac kground concept. The underlying theory of the model relies on a series of a ssumptions that link psychophysically determined detection thresholds to co ne phototransduction. Correction of thresholds for the reduced quantum-catc hing ability of the cones (due to the depletion of photopigment caused by a bleaching light) is an important aspect of the model. 3. Foveal detection thresholds were measured for a small test flash present ed on a large steady background field or presented alone after adapting to the background field. Test and background fields were monochromatic, with w avelengths closely matched to promote detection by the luminance mechanism. 4. The model provided a good description of the data collected under these conditions. Parameters of the model were similar for all wavelengths and ea ch observer, as were the derived equivalent background relationships. Analy sis of previously published data for Stiles' pi (5) mechanism gave analogou s results. 5. The model is made up of two components. The early (fast) component is li kely to be due to the direct action of the cone equivalent of inactivated R h* on the G-protein cascade and/or the reverse reaction of the cone equival ent of inactivated Rh* to Rh*. The later (slow) component may be due to the direct action of cone opsin on the G-protein cascade.