Changes of inner retina under different ischemic reperfusion induced by acute intraocular hypertension in rats
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Purpose of review Several studies have shown that the pattern electroretinogram, a direct, objective method of measuring retinal ganglion cell function, is altered early in ocular hypertension and glaucoma. Renewed interest in the pattern electroretinogram for early detection of pre-perimetric glaucoma has been sparked by noninvasive and reproducible methods of recording using skin electrodes. Recent findings With the noninvasive pattern electroretinogram, response abnormalities have been detected in up to 50% of glaucoma suspects with normal standard perimetry. In early glaucoma (with either normal or high intraocular pressure), a reduction of intraocular pressure has sometimes yielded improvement in pattern electroretinogram amplitude. A prolonged steady-state stimulus presentation reduces the pattern electroretinogram amplitude and increases optic nerve blood flow in normal subjects, suggesting that sustained activity of retinal ganglion cells is physiologically associated with autoregulatory changes of the neural-vascular system. It is unknown whether this autoregulation is altered in glaucoma. The multifocal pattern electroretinogram does not seem to have an advantage over the pattern electroretinogram in the early detection of glaucoma. The photopic negative response of the diffuse flash electroretinogram has shown changes in glaucoma, but may not be able to detect retinal dysfunction in normal tension glaucoma. Summary The pattern electroretinogram is a noninvasive, direct, objective method that may be useful to clinicians in detecting early retinal ganglion cell dysfunction in glaucoma suspects. The pattern electroretinogram may also optimize treatment strategies based on improvement of retinal ganglion cell function.
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Early retinal neurodegeneration occurs as one of the complications of diabetes even before clinically detectable diabetic vascular retinopathy. The pathogenesis of retinal diabetic neuropathy is still not well understood. We investigated the serial changes or fluctuations in intraocular pressure (IOP) and examined their roles in the pathogenesis of neuronal degeneration in diabetic retina.Male Sprague Dawley rats with streptozotocin-induced diabetes were treated with ophthalmic preparations of brinzolamide, latanoprost, both drugs (combined treatment) or saline for 8 weeks. IOP was measured daily under general anaesthesia using a rebound tonometer. Antegrade axoplasmic flow in the optic nerve was assessed with a fluorescent substrate. Immunohistochemical staining, TUNEL assays and western blots were also used.The fluctuation of IOP was higher in the diabetes group than in the normal control or the combined treatment group. Diabetes-induced apoptosis of retinal ganglion cells was decreased by combined treatment. Increased expression of glial fibrillary acidic protein or Iba-1 in the retina or optic nerve head, induced by diabetes, was attenuated only by the combined treatment. Intercellular adhesion molecule-1 was increased in diabetic rats but not in the combined treatment group. Diabetes-induced loss of antegrade axoplasmic transport was partially relieved with combined treatment.Elevated IOP fluctuations seemed to be associated with the gliosis, neuroinflammation, and neurodegeneration induced by diabetes. The loss of retinal ganglion cells might be relieved by IOP-lowering medication. The improvement of unstable perfusion pressure could play a role in neuroprotection in the diabetic retina.
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Ocular hypertension is a primary risk factor for glaucoma and results in retinal ganglion cell (RGC) degeneration. Current animal models of glaucoma lack severe RGC cell death as seen in glaucoma, making assessment of physiological mediators of cell death difficult. We developed a modified mouse model of ocular hypertension whereby long-lasting elevation of intraocular pressure (IOP) is achieved, resulting in significant reproducible damage to RGCs.In this model, microbeads are mixed with hyaluronic acid and injected into the anterior chamber of C57BL/6J mice. The hyaluronic acid allows for a gradual release of microbeads, resulting in sustained blockage of Schlemm's canal. IOP elevation was bimodal during the course of the model's progression. The first peak occurred 1 hours after beads injection, with an IOP value of 44.69 ± 6.00 mmHg, and the second peak occurred 6-12 days post-induction, with an IOP value of 34.91 ± 5.21 mmHg. RGC damage was most severe in the peripheral retina, with a loss of 64.1% compared to that of untreated eyes, while the midperiphery exhibited a 32.4% loss, 4 weeks following disease induction.These results suggest that sustained IOP elevation causes more RGC damage in the periphery than in the midperiphery of the retina. This model yields significant and reproducible RGC degeneration.
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