PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11483176

Multiple processes mediate flicker sensitivity.

A J Anderson·A J Vingrys
View original source ↗Export metadata ↓

Abstract

By systematically manipulating the luminance of a flickering spot and the area immediately surrounding it, we investigated why thresholds from flickering stimuli that cause a change in average luminance are elevated relative to those from stimuli with no luminance change. Threshold elevation resulted from local light adaptation and from temporal-frequency-specific interactions between the spot and its surround: at low frequencies, the contrast between the spot and the surround elevated thresholds, whereas at high frequencies, dark adaptation within the surround elevated thresholds. Our findings suggest that two common ways of determining temporal sensitivity may give markedly different outcomes.

Explore related subjects

Adaptation, OcularAdultAnalysis of VarianceContrast SensitivityHumansLightingSensory ThresholdsTime FactorsJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A J Anderson, A J Vingrys. 2001. Multiple processes mediate flicker sensitivity.. https://doi.org/10.1016/s0042-6989(01)00139-0

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Lazy eyes zebrafish mutation affects Müller glial cells, compromising photoreceptor function and causing partial blindness.

A behavioral assay based on the optokinetic reflex was used to screen chemically mutagenized zebrafish larvae for deficits in visual function. A homozygous recessive mutation, lazy eyes (lze), was isolated based on the observation that 5-day postfertilization (dpf) mutants displayed weaker and less frequent eye movements than wild-type fish in response to moving stripes. Electroretinographic (ERG) recordings revealed that mutants had severely reduced a- and b-wave amplitudes relative to wild-type fish, indicating outer retinal dysfunction. Retinal lamination and cellular differentiation were normal in the lze retina; however, mutant photoreceptor cells had small outer segments and pyknotic nuclei were occasionally observed in the outer retina and the marginal zone of lze. Cone, rod, amacrine, bipolar, and Müller cell marker analyses indicated that the typical lze retina contained fewer rod photoreceptors and fewer Müller cells than wild-type fish at 5 dpf. At 3 dpf, however, mutant retinas had normal numbers of rod photoreceptors and Müller cells, suggesting that the initial differentiation of these cell types occurred normally. Rod photoreceptor histology was normal at this early stage, but Müller cells were often hypertrophied, suggesting that they were unhealthy. Constant light rearing of mutant animals accelerated the Müller cell degeneration, severely worsened the visual deficit, but had no obvious affect on the photoreceptors. When ERG responses and Müller cell degeneration from the same mutant animals were analyzed, the extent of the Müller cell loss matched closely the degree to which ERG responses were reduced. In summary, the lze gene appears to be required for Müller cell viability and normal visual function. The lze mutant may be a model for the study of the involvement of Müller cells in photoreceptor development and function.

Adaptation, Ocular↗
PubMed2003

Sensorimotor adaptation to visual distortions with different kinematic coupling.

We investigated the mechanisms of sensorimotor adaptation by sequentially exposing human subjects to different visual distortions. Subjects performed a manual tracking task, while the relationship between their actual finger movement and its visual feedback was manipulated either by a position-to-position (PP), or by a position-to-velocity (PV) transformation. The outcome confirmed previous findings, in that adaptation to PP facilitated the subsequent adaptation to a second, additional PP. More importantly, our present data documented that pre-exposure to PP interferes with the subsequent adaptation to PV, and vice versa. Thus, we observed anterograde interference between two transformations of common physical nature (i.e., visual), but different kinematic coupling. When previous work on sequential adaptation to visual and mechanical transformations is reconsidered in light of this finding, converging evidence is yielded in favor of a distributed adaptive mechanism, where the magnitude of interference between two successive adaptation sessions depends on the overlap of the involved neural structures.

Adaptation, Ocular↗
PubMed2003

Light adaptation through phosphoinositide-regulated translocation of Drosophila visual arrestin.

Photoreceptor cells adapt to bright or continuous light, although the molecular mechanisms underlying this phenomenon are incompletely understood. Here, we report a mechanism of light adaptation in Drosophila, which is regulated by phosphoinositides (PIs). We found that light-dependent translocation of arrestin was defective in mutants that disrupt PI metabolism or trafficking. Arrestin bound to PIP(3) in vitro, and mutation of this site delayed arrestin shuttling and resulted in defects in the termination of the light response, which is normally accelerated by prior exposure to light. Disruption of the arrestin/PI interaction also suppressed retinal degeneration caused by excessive endocytosis of rhodopsin/arrestin complexes. These findings indicate that light-dependent trafficking of arrestin is regulated by direct interaction with PIs and is required for light adaptation. Since phospholipase C activity is required for activation of Drosophila phototransduction, these data point to a dual role of PIs in phototransduction.

Adaptation, Ocular↗