Time course of chromatic adaptation for color appearance and discrimination.
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Adaptation to a steady background has a profound effect on both color appearance and discrimination. We determined the temporal characteristics of chromatic adaptation for appearance and discrimination along different color directions. Subjects were adapted to a large uniform background made up of a CRT screen and a 45x64 degrees wall, illuminated by computer controlled lamps. After an instant change in background color along a red-green or blue-yellow color axis, we measured thresholds for the detection of increments along the same axes at fixed times between 25 ms and 121 s. Analogously, color appearance was determined using achromatic matching. Three components of adaptation could be identified by their temporal characteristics. A slow exponential time course of adaptation with a half-life of about 20 s was common to appearance and discrimination. A faster component with a half-life of 40-70 ms--probably due to photoreceptor adaptation--was also common to both. Exclusive for color appearance, there was a third, extremely rapid mechanism with a half-life faster than 10 ms. This instantaneous process explained more than 50% of total adaptation for color appearance and could be shown to act in a multiplicative manner. We conclude that this instantaneous adaptation mechanism for color appearance is situated at a later processing stage, after mechanisms common to appearance and discrimination, and is based on multiplicative spatial interactions rather than on local, temporal adaptational processes. Color appearance, and thus color constancy, seems to be determined in large part by cortical computations. (+info)
Synaptic activity of frog retinal photoreceptors. A peroxidase uptake study.
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The uptake of horseradish peroxidase (HRP) into membranous structures, detectable by light and electron microscopy, is used here to monitor the synaptic activity of photoreceptors of isolated frog retinas maintained in the dark or under various illumination conditions. The major findings are: (a) Neurotransmission from photoreceptor terminals seems to involve the same types of endocytic membrane-retrieval processes that occur at other nerve terminals. Presumably, the endocytic processes compensate for exocytic events associated with neurotransmission. The retrieved membrane is "recycled" to form vesicles. Some of these accumulate near the synaptic ribbons, perhaps indicating reutilization for exocytosis. On the other hand, some retrieved membrane evidently is degraded via multivesicular bodies that appear to undergo "retrograde" transport from the receptor synapses to the myoid regions. (b) Photoreceptor terminals take up much HRP in the dark. Steady illumination markedly decreases uptake by rods. Uptake by cones is notably reduced only at illumination intensities higher than those that have maximal effects on rods. (c) The decrease in rod HRP uptake with light is reversible when retinas are allowed to adapt to the dark, if the light exposures used were at intensities that bleach very little visual pigment. Such "recovery" is not observed after light exposures that bleach a considerable amount of visual pigment. The cones recover their dark levels of HRP uptake even after light exposures that bleach considerable amounts of visual pigment. The changes in HRP uptake that we observe parallel expectations for photoreceptor synaptic neurotransmission derived from indirect physiological evidence. (+info)
Diagnostic features of the Favre-Goldmann syndrome.
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Extensive retinal vascular disease was noted in three patients from two families with Favre-Goldmann syndrome. In addition to classical features they had pronounced leakage from some retinal vessels. Vessels were either opaque ('sclerotic') or non-perfused. Cystoid macular oedema was a contributing cause of decreased vision. Two of the three patients showed a discrepancy on electroretinography between single-flash photopic amplitudes and flicker fusion frequency. This may be characteristic of Favre-Goldmann syndrome. (+info)
The formation of metarhodospin380 in the retinal rods of the frog.
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1. The formation of metarhodopsin380 (metarhodopsin II) was studied in isolated frog retinas exposed to intense flashes of 120 mus duration. 2. A rapid increase in absorbance at 375 nm during the flash was followed by a slower absorbance increase in the subsequent dark period. The slower increase showed virtual completion after 5 ms. 3. The fast absorbance increase during the flash was due to the formation of metarhodopsin478. The rate of this reaction was dependent on the time course of the flash and on the decay rate of lumirhodopsin. 4. Kinetic analysis indicates that three consecutive reactions occur: the light-controlled formation of lumirhodopsin, its first-order decay to metarhodopsin478 and the conversion of metarhodopsin478 into metarhodopsin380. At 21 degrees C, the decay constants were 2 X 10(4) S-1 (lumirhodopsin) and 1 X 10(3) S-1 (metarhodopsin478), respectively. (+info)
The histidine kinase-related domain participates in phytochrome B function but is dispensable.
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Phytochromes are photoreceptors that control many plant light responses. Phytochromes have two carboxyl-terminal structural domains called the PAS repeat domain and the histidine kinase-related domain. These domains are each related to bacterial histidine kinase domains, and biochemical studies suggest that phytochromes are light-regulated kinases. The PAS repeat domain is important for proper phytochrome function and can interact with putative signaling partners. We have characterized several new phytochrome B mutants in Arabidopsis that express phyB protein, three of which affect the histidine kinase-related domain. Point mutations in the histidine kinase-related domain cause phenotypes similar to those of null mutants, indicating that this domain is important for phyB signaling. However, a truncation that removes most of the histidine kinase-related domain results in a phyB molecule with partial activity, suggesting that this domain is dispensable. These results suggest that phytochromes evolved in modular fashion. We discuss possible functions of the histidine kinase-related domain in phytochrome signaling. (+info)
A brief review of retinitis pigmentosa and the identified retinitis pigmentosa genes.
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The family of inherited ocular diseases that is collectively known as retinitis pigmentosa is a major cause of progressive retinal disease worldwide. As such, this family of diseases has been the object of much scientific scrutiny, both clinical and basic. The recent application of molecular genetic analyses has heralded the rapid elucidation of the underlying gene defects in many cases. In this article, the fundamental clinical and electroretinographic characteristics of retinitis pigmentosa will be recalled. Additionally, the current understanding of the genetic causes of retinitis pigmentosa will be reviewed, and the identified causative genes will be classified into groups related by function. (+info)
Sustained but not transient phytochrome A signaling targets a region of an Lhcb1*2 promoter not necessary for phytochrome B action.
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Current evidence is inconclusive regarding the point of signaling convergence downstream from different members of the phytochrome family. In transgenic Arabidopsis, the activity of a reporter enzyme under the control of the -453 to +67 fragment of an Lhcb1*2 promoter shows very low fluence responses (VLFRs) and high-irradiance responses (HIRs) mediated by phytochrome A and low-fluence responses (LFRs) mediated by phytochrome B. A 5' deletion of the promoter to -134 abolished the HIR without affecting VLFR or LFR. In transgenic tobacco, VLFR and LFR were observed for the -176 to -31 or -134 to -31 fragments of Lhcb1*2 fused to 35S cauliflower mosaic virus minimal promoters, but only the largest fragment showed HIR. We propose that sustained activation of phytochrome A with far-red light initiates a signaling cascade that deviates from phytochrome B signaling and transient phytochrome A signaling and that this divergence extends as far as the Lhcb1*2 promoter. (+info)
GIGANTEA is a nuclear protein involved in phytochrome signaling in Arabidopsis.
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In a genetic screen of available T-DNA-mutagenized Arabidopsis populations for loci potentially involved in phytochrome (phy) signaling, we identified a mutant that displayed reduced seedling deetiolation under continuous red light, but little if any change in responsiveness to continuous far-red light. This behavior suggests disruption of phyB, but not phyA signaling. We have cloned the mutant locus by using the T-DNA insertion and found that the disrupted gene is identical to the recently described GIGANTEA (GI) gene identified as being involved in control of flowering time. The encoded GI polypeptide has no sequence similarity to any known proteins in the database. However, by using beta-glucuronidase-GI and green fluorescent protein-GI fusion constructs, we have shown that GI is constitutively targeted to the nucleus in transient transfection assays. Optical sectioning by using the green fluorescent protein-GI fusion protein showed green fluorescence throughout the nucleoplasm. Thus, contrary to previous computer-based predictions that GI would be an integral plasma membrane-localized polypeptide, the data here indicate that it is a nucleoplasmically localized protein. This result is consistent with the proposed role in phyB signaling, given recent evidence that early phy signaling events are nuclear localized. (+info)