PurposeModerately elevated intraocular pressure (IOP) is a risk factor for open-angle glaucoma. Some patients suffer glaucoma despite clinically measured normal IOPs. Fluctuations in IOP may have a significant role since IOPs are higher during sleep and inversion activities. Controlled transient elevations of IOPs in rats over time lead to optic nerve structural changes that are similar to the early changes observed in constant chronic models of glaucoma. Because early intervention decreases glaucoma progression, this study was done to determine if early physiological changes to the retina could be detected with noninvasive electrophysiological and optical imaging tests during moderately elevated IOP.MethodsIntraocular pressures were raised to moderately high levels (35 mm Hg) in one eye of Sprague-Dawley rats while the other (control) eye was untreated. One group of rats underwent scotopic threshold response (STR) and electroretinogram (ERG) testing, while another 3 groups underwent optical coherence tomography (OCT) imaging, Western blot, or histologic evaluation.ResultsThe amplitudes of the STR and ERG responses in eyes with moderately elevated IOPs were enhanced compared to the values before IOP elevation, and compared to untreated contralateral eyes. Structural changes to the optic nerve also occurred during IOP elevation.ConclusionsAlthough ischemic IOP elevations are well-known to globally reduce components of the scotopic ERG, acute elevation in rats to levels often observed in untreated glaucoma patients caused an increase in these parameters. Further exploration of these phenomena may be helpful in better understanding the mechanisms mediating early retinal changes during fluctuating or chronically elevated IOP.
Visually evoked intrinsic optical signals (IOSs) were measured in vivo for the first time to our knowledge from all retina layers of the chicken retina with a combined functional optical coherence tomography and electroretinography (ERG) system. IOS traces were recorded from a small volume in the retina with 3.5 μm axial resolution and 7 ms time resolution. Comparison of the IOS and ERG traces shows a correlation between the positive and negative IOS measured from different retinal layers and the timing of the a and b waves in the ERG recording.
UHR-OCT permits in vivo, noninvasive, longitudinal, quantitative assessment of the progressive changes in retinal morphology and optical reflectivity in a sodium iodate rodent model of outer retinal degeneration.
The consistent results of the sucrose solution tests suggest that the ocular mass density is a physical property that is more dependent on the compositional and structural characteristics of the tissue and than on population variability.
To test the hypothesis that the same mechanisms mediate form deprivation and lens-induced myopia, the ocular growth responses of chicks alternately exposed to lenses and diffusers at regular intervals (3h) were compared to those of chicks exposed to either negative lenses or diffusers alone. In total, there were four experiments: (1) -15 D lenses and/or diffusers on normal birds, (2) -15 D lenses and/or diffusers on optic nerve-sectioned (ONS) birds, (3) -5/-10/-15 D lenses (sequentially applied) and/or diffusers on normal birds and (4) -5/-10/-15 D lenses and/or diffusers on ONS birds. All treatments were monocular. In all experiments, optical axial lengths (cornea-to-retina distances) in treated eyes were greater than in fellow eyes, irrespective of the optical device (diffuser, lens or switch), lens power (fixed or incremented) and optic nerve condition (intact or severed). In normal chicks, optical axial length responses in the switch group were significantly reduced relative to those of the diffuser but not to those of the -15 D lens group. For both groups of ONS birds, diffusers exaggerated the optical axial length changes. For all groups, the responses to the switch and lens groups were most similar. These results together suggest that the mechanisms mediating form deprivation- and lens-induced myopia are different.
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