No abstract

Although influenced by CCT, iCare agrees well with applanation tonometers.

In mammals, intrinsically photosensitive retinal ganglion cells (ipRGCs) mediate non-image-forming visual functions such as pupillary light reflex (PLR) and circadian photoentrainment. This photosensitivity requires melanopsin, an invertebrate opsin-like protein expressed by the ipRGCs. The precise role of melanopsin remains uncertain. One suggestion has been that melanopsin may be a photoisomerase, serving to regenerate an unidentified pigment in ipRGCs. This possibility was echoed by a recent report that melanopsin is expressed also in the mouse retinal pigment epithelium (RPE), a key center for regeneration of rod and cone pigments. To address this question, we studied mice lacking RPE65, a protein essential for the regeneration of rod and cone pigments. Rpe65 ؊/؊ ipRGCs were Ϸ20-to 40-fold less photosensitive than normal at both single-cell and behavioral (PLR) levels but were rescued by exogenous 9-cis-retinal (an 11-cis-retinal analog), indicating the requirement of a vitamin A-based chromophore for ipRGC photosensitivity. In contrast, 9-cis-retinal was unable to restore intrinsic photosensitivity to melanopsin-ablated ipRGCs, arguing against melanopsin functioning merely in photopigment regeneration. Interestingly, exogenous all-trans-retinal was also able to rescue the low sensitivity of rpe65 ؊/؊ ipRGCs, suggesting that melanopsin could be a bistable pigment. Finally, we detected no melanopsin in the RPE and no changes in rod and cone sensitivities due to melanopsin ablation. Together, these results strongly suggest that melanopsin is the photopigment in the ipRGCs.RPE65 ͉ chromophore M elanopsin, an opsin-like protein, was first identified in dermal melanophores of Xenopus laevis (1) and subsequently was found in a small subset of retinal ganglion cells that is intrinsically photosensitive in mammals (2, 3). These intrinsically photosensitive retinal ganglion cells (ipRGCs) project predominantly to the suprachiasmatic nucleus (SCN), the intergeniculate leaflet, and the olivary pretectal nucleus (OPN) of the brain (3). These nuclei are important for circadian photoentrainment and the pupillary light reflex (PLR), accessory visual functions reporting ambient luminance rather than image formation on the retina. In melanopsin-knockout (opn4 Ϫ/Ϫ ) mice, the ipRGCs are present in normal numbers and project to the correct targets in the brain but are no longer intrinsically photosensitive (4). Thus, melanopsin is required for light detection by these cells. The PLR of opn4 Ϫ/Ϫ mice is also incomplete (4), and their circadian photoentrainment is attenuated (5, 6). In mice lacking both melanopsin and functional rods and cones, the PLR and circadian photoentrainment are abolished (7,8). Thus, the melanopsin-associated and rod-cone photoreceptive systems appear to account for all major non-image-forming visual functions.The action spectrum of the light response of ipRGCs can be fit by the absorption spectrum of a vitamin A-based photopigment with peak absorbance ( max ) at Ϸ484 nm (2). This action spectrum closel...

Cone bipolar cells of the vertebrate retina connect photoreceptors with ganglion cells to mediate photopic vision. Despite this important role, the mechanisms that regulate cone bipolar cell differentiation are poorly understood. VSX1 is a CVC domain homeoprotein specifically expressed in cone bipolar cells. To determine the function of VSX1, we generated Vsx1 mutant mice and found that Vsx1 mutant retinal cells form but do not differentiate a mature cone bipolar cell phenotype. Electrophysiological studies demonstrated that Vsx1 mutant mice have defects in their cone visual pathway, whereas the rod visual pathway was unaffected. Thus, Vsx1 is required for cone bipolar cell differentiation and regulates photopic vision perception.

Purpose: To evaluate the relationship between age and retinal nerve fiber layer (RNFL) thickness in normal subjects, as measured by optical coherence tomography (OCT). Methods: One hundred and forty-four normal subjects (144 eyes), ranging from 16 to 84 years of age, were enrolled in this cross-sectional study. The RNFL thickness was determined using OCT with three circle scans 3.4 mm in diameter. Results: The average RNFL thickness was inversely correlated with age (r = –0.348, p < 0.001). Analyzing the quadrants as a parameter, RNFL thickness in the superior, temporal and inferior quadrants also decreased with age. Using 30-degree segments, there were significant correlations between age and the RNFL thickness of temporal segments (7–11 o’clock). The average RNFL thickness had the highest correlation among all parameters (r = –0.348, p < 0.001). Regarding nasal quadrant thickness, RNFL ratios (average, superior, temporal and inferior RNFL thickness relative to the nasal quadrant thickness) were not significantly correlated with age. The refractive error did not affect RNFL thickness (r = 0.091, p = 0.276). Conclusion: Our study revealed that RNFL thickness, in particular in the temporal quadrant, measured by OCT significantly decreased with age. Age has to be taken into consideration when we compare RNFL thickness between normal and glaucomatous eyes.

There is a threshold nonlinearity operating at the output of the rod to rod bipolar cell synapse that can usefully reduce the transmission of continuous rod noise without significantly affecting the transmission of single-photon signals. This nonlinearity does not affect the overall linear function of the rod pathway at levels at which it is effectively operating in a photon-counting mode.

The vertebrate retina develops from an amorphous sheet of dividing retinal progenitor cells (RPCs) through a sequential process that culminates in an exquisitely patterned neural tissue. A current model for retinal development posits that sequential cell-type differentiation is the result of changes in the intrinsic competence state of multipotent RPCs as they advance in time and that the intrinsic changes are influenced by continuous changes in the extracellular environment. Although several studies support the proposition that newly differentiated cells alter the extrinsic state of the developing retina, it is still far from clear what role they play in modifying the extracellular environment and in influencing the properties of RPCs. Here, we specifically ablate retinal ganglion cells (RGCs) as they differentiate, and we determine the impact of RGC absence on retinal development. We find that RGCs are not essential for changing the competence of RPCs, but they are necessary for maintaining sufficient numbers of RPCs by regulating cell proliferation via growth factors. Intrinsic rather than extrinsic factors are likely to play the critical roles in determining retinal cell fate.

DM has an additive effect on apoptosis induction by chronic elevation of IOP. Diabetes may act as a risk factor of open-angle glaucoma by increasing susceptibility of retinal cells including retinal ganglion cells to apoptosis triggered by additional stresses such as elevated IOP.