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These exampies contrast with the electrical responses of arthropod photoreceptor cells, in which illumination leads to an enzyme cascade that activates photoreceptor cell currents (e.g., in Drosophila via the opening of TRP channels; Minke and Selinger, 1996); and, conversely, currents are turned off by channel closure upon removal of illumination.
Photoreceptor cells in the retina sense light, signaling the brain, but only in the presence of retinal molecules within the cells.
Calcium-induced calpain mediates apoptosis via caspase-3 in a mouse photoreceptor cell line.
Retinal degenerative diseases such as retinal pigmentosa and age-related macular degeneration (AMD) are the major causes of vision loss due to cell death or functional loss of photoreceptor cells (PRCs) and/or retinal pigment epithelium (RPE) [1].
The most common pathway of retinitis pigmentosa results from a primary defect in the rod photoreceptor cascade, a specific biochemical pathway that transduces light and leads to changes in photoreceptor cell polarization.
Our histological analysis revealed that spermidine initially induced RPE cell damage and degeneration, whereas photoreceptor cell death was a secondary outcome.
Our results are consistent with the observation by Noell (1980); that is, retinal neuronal cell DNA levels are correlated with ERG b-wave estimates of photoreceptor cell loss in light-exposed retinals of rats.
Visual photoreceptor cells in the retina are of two types: rods and cones.
the number and subcellular morphology of photoreceptor cells (PRCs), their spatial distribution and the physical dimensions and arrangements of their photoreceptor membranes.
Mechanisms addressed here include diabetes, statins, Drusen, RPE lipofuscin, genetic modifiers, X-linked retinal dystrophies and synaptic remodeling, while therapeutic strategies include the suppression of photoreceptor cell death, cell-based therapies, IPE transplantation, retinal transplantation, stem cells, encapsulated cell technology, neuroprotective factors, and carbon anhydrase inhibitors.
Histologic studies of eyes with retinal vein occlusion showed that cystoid spaces in ME associated with BRVO often in the outer nuclear layer and causes liquefaction necrosis of cells, which results in photoreceptor cell loss and dysfunction in the fovea [6].
It is also detected in vesicles distributed throughout the photoreceptor cell body, which suggests that LpOps6 is shed from rhabdoms (Battelle et al., 2015).