Disease relevance of Adaptation, Ocular

• Sensitivity-modulating protein (S-modulin) is a Ca(2+)-binding protein involved in light adaptation in frog rods; it regulates both the light sensitivity of PDE and the lifetime of activated PDE by controlling rhodopsin phosphorylation in a Ca(2+)-dependent manner [1].
• Since dopamine is especially involved in light adaptation from darkness, the residual retina could act in triggering the turning behavior of Proteus in response to lightening [2].
• Furthermore, Na+ channel modulation is implicated in the control of input-output relationships in several types of neuron and seems to be involved in phenomena as varied as cocaine withdrawal, hyperalgesia and light adaptation [3].

Psychiatry related information on Adaptation, Ocular

• These results suggest a role for the ryanodine receptor in both a cellular correlate of classical conditioning and light adaptation [4].

High impact information on Adaptation, Ocular

• The intensity dependence of the photoresponse in rods lacking arrestin further suggests that, although arrestin is required for normal signal termination, it does not participate directly in light adaptation [5].
• We now show that under physiological conditions light adaptation is severely reduced in inaC, suggesting that eye-specific PKC, itself activated by a rise in cytosolic calcium and diacylglycerol, is required for adaptation [6].
• On the basis of these studies, Ca2+ is suggested to play a central role in photorecovery and light adaptation, not only by regulating guanylate cyclase, possibly through recoverin, but also by modulating the cGMP-gated channel through calmodulin interaction with the 240K protein [7].
• This is believed to be one of the mechanisms of light-adaptation produced by activation of guanylate cyclase [8].
• Similarly, 'light adaptation' involves decreased coupling of photoactivated rhodopsin to cGMP phosphodiesterase activation [9].

Biological context of Adaptation, Ocular

• These data appear to exclude models for light adaptation that postulate high levels of phosphorylation of non-bleached rhodopsin in rod photoreceptors [10].
• Interactions between arrestins and phosphoinositides have been reported to regulate multiple membrane-associated signaling and trafficking events including clathrin-mediated endocytosis and light adaptation in Drosophila [11].
• Injection of EGTA into a retinula cell maintained a steady state of light adaptation, was found to cause an increase in amplitude and duration of the response to a short test flash, thus producing the effects of dark adaptation [12].
• Long-term (greater than 15 min) exposures to GABA and picrotoxin elicited changes in response kinetics usually associated with dark and light adaptation, respectively [13].
• At the highest usable levels of light adaptation, the latencies of receptor potentials from cells exposed only to sea water containing chlorobutanol were virtually identical [14].

Anatomical context of Adaptation, Ocular

• Calmodulin regulation of light adaptation and store-operated dark current in Drosophila photoreceptors [15].
• Triton X-100 solubilized monomers of bacteiorhodopsin (bR) show a decrease in the extent of light adaptation; the red shift and the absorbance increase of the visible absorption band are reduced no less than half the values observed in purple membrane (p.m.) with a corresponding reduction in the isomerization of 13-cis- to all-trans-retinal [16].
• In the rabbit, light adaptation enhanced NADPH diaphorase activity in amacrine cells and practically eliminated it in horizontal cells [17].
• The combination 10(-3) M ALA with 10(-6) M melatonin inhibited retinal porphyrin synthesis after green light adaptation, while in the pigment epithelium green light adaptation induced porphyrin synthesis [18].
• State transitions and light adaptation require chloroplast thylakoid protein kinase STN7 [19].

Associations of Adaptation, Ocular with chemical compounds

• It is well established that during light adaptation, the amount of retinol drops in the NR but rises in the RPE [20].
• As well as being a major charge carrier for the light-induced current, Ca2+ influx via the trp-dependent channels appears to be required for refilling Ca2+ stores sensitive to inositol 1,4,5-trisphosphate and for feedback regulation (light adaptation) of the transduction cascade [21].
• The reduction in retinal dopamine is evident only during light adaptation and is accompanied by a decreased rate of dopamine biosynthesis [22].
• We describe here that the effects of retinoic acid on these properties are similar to those of light adaptation [23].
• The formation of these spinules during light adaptation is impaired in the presence of citral, a competitive inhibitor of the dehydrogenase responsible for the generation of retinoic acid in vivo [23].

Gene context of Adaptation, Ocular

• These findings indicate that light-dependent trafficking of arrestin is regulated by direct interaction with PIs and is required for light adaptation [24].
• Localization of heme oxygenase in rat retina: effect of light adaptation [25].
• A key component in dark/light adaptation is phosducin, a phosphorylatable protein that modulates the amount of transducin heterotrimer (Gt alpha beta gamma) available through sequestration of the beta gamma subunits (Gt beta gamma) [26].
• In this system, we investigate the hitherto unknown physiological roles of calmodulin (CaM) in light adaptation and in regulation of the inward current that is brought about by depletion of cellular Ca2+ stores [15].
• The results indicate that light adaptation is primarily mediated downstream of PLC and independently of PKC by Ca(2+)-dependent inhibition of TRP channels [27].

Analytical, diagnostic and therapeutic context of Adaptation, Ocular

• Electroretinograms were recorded for 23 monochromatic stimuli (400-700 nm) at an equal energy with white light adaptation before and after treatment with the glutamate analogues, 2-amino-4-phosphonobutyric acid, cis -2,3-piperidine-dicarboxylic acid, or both [28].
• Conformation changes were monitored by circular dichroism as a function of light adaptation and solvent composition (hexafluoroisopropanol [HFIP] vs trifluoroethanol [TFE]) [29].
• In a double-blind placebo crossover study of 13 healthy volunteers, the pineal hormone melatonin (10 mg) was given at 4 pm, and the electroretinogram measured under conditions of dark and light adaptation [30].
• The localization of the S-antigen was studied by electron microscopy in the rabbit eye, under three conditions of adaptation: A) 24-hour dark adaptation, B) 24-hour dark adaptation and 1.5-hour light adaptation and C) light adaptation for 30 hours [31].

References