Changes in the oscillatory potentials of the electroretinogram in glaucoma

Gur, Moshe; Zeevi, Yehoshua Y.; Bielik, Magda; Neumann, E.

doi:10.3109/02713688709025202

Cited by 43 publications

(31 citation statements)

References 12 publications

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“…A reduction of OPs in patients with glaucoma or optic nerve diseases has been reported (Gur 1987;Vaegan 1995) but this does not necessarily correlate with the extent of damage in individual patients. It has been suggested (Vaegan 1991;Vaegan 1994;Vaegan 1995) that changes in the ganglion cell dendrites might cause the reduction in OPs.…”

Section: Discussionmentioning

confidence: 99%

Characterization of retinal damage in the episcleral vein cauterization rat glaucoma model

Danias

Shen

Kavalarakis

et al. 2006

Experimental Eye Research

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Episcleral vein cauterization (EVC) is used in rats to generate a glaucoma model with high intraocular pressure (IOP). The long-term retinal damage in this glaucoma model however, has not been accurately quantified. We report the location and amount of retinal ganglion cell (RGC) damage caused by (EVC) induced IOP elevation in two rat strains.IOP was raised in one eye of Wistar(N=5) and Brown-Norway(B-N)(N=7) rats by EVC and monitored monthly until IOP in contralateral eyes equalized at 5 months post-surgery. Animals were maintained for 3.5-4.5 additional months. B-N rats(N=7) that had no EVC served as controls for this strain. Scotopic flash ERGs were recorded at baseline and just prior to euthanasia. Automated counts of all retrogradely labeled RGCs in retinal flat-mounts were determined and compared between contralateral eyes. RGC density maps were constructed and RGC size distribution was determined.Oscillatory potentials in the group of eyes which had elevated IOP were decreased at the time of euthanasia, when IOP had returned to normal. A group of normal B-N rats had similar RGC counts between contralateral eyes. In the experimental group the mean number of RGCs was not significantly different between control and experimental eyes, but 1 of 5 Wistar and 2 of 7 B-N experimental eyes had at least 30% fewer RGCs from contralateral control eyes. Total retinal area in B-N experimental eyes was higher compared with contralateral eyes. Cumulative IOP exposure of the experimental eyes was modestly correlated with RGC loss while oscillatory potentials appeared to be inversely related to RGC loss. In retinas with extensive (>30% RGC loss) but not complete damage, smaller cells were preserved better than larger ones.The above results indicate that RGC loss in both Wistar and B-N strains is variable after a prolonged elevation of IOP via EVC. Such variability despite equivalent IOP levels and ERG abnormalities, suggests unknown factors that can protect IOP-stressed RGCs. Identification and enhancement of such factors could prove useful for glaucoma therapy.

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Section: Discussionmentioning

confidence: 99%

Characterization of retinal damage in the episcleral vein cauterization rat glaucoma model

Danias

Shen

Kavalarakis

et al. 2006

Experimental Eye Research

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“…Some reports have challenged the belief that the¯ash ERG is essentially normal after optic nerve damage or in glaucoma, as discussed by Korth (1997). These reports demonstrated that glaucoma can affect components of thē ash ERG, such as scotopic ERG amplitude and implicit time changes (Alvis, 1966;Ogata, 1976;Wanger and Persson, 1983;Fazio et al, 1986;Lambrou and Greve, 1989), an altered scotopic threshold response (Korth, Nguyen and Martus, 1994;Frishman et al, 1996), changes in oscillatory potentials (Gur et al, 1987;Vaegan et al, 1995), reduced responses to¯icker (Alvis, 1966;Holopigian et al, 1990;Odom et al, 1990), and reduced cone-mediated ERG b-wave amplitude and prolonged implicit times (Holopigian et al, 1990;Vaegan et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Electroretinographic Abnormalities in a Rat Glaucoma Model with Chronic Elevated Intraocular Pressure

Bayer

Danias

Brodie

et al. 2001

Experimental Eye Research

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“…Consistent with this, a decrease in the amplitude of oscillatory potentials, presumed to be generated by amacrine cells, has been reported in human glaucomatous eyes. 62 Future studies should address the functional status of amacrine cells following microvasculature loss in glaucoma.…”

Section: Discussionmentioning

confidence: 99%

Acetylcholinesterase Inhibition Promotes Retinal Vasoprotection and Increases Ocular Blood Flow in Experimental Glaucoma

Almasieh

Macintyre

Pouliot

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. A clear correlation between vascular deficits and retinal ganglion cell (RGC) loss in glaucoma has not yet been established. The question arose as to whether there is loss of inner retinal vessels following intraocular pressure (IOP) increase and, if so, whether it occurs prior to, concomitantly with, or after RGC death. We also sought to establish whether galantamine, an acetylcholinesterase inhibitor that promotes RGC survival, can protect the retinal microvasculature and enhance blood flow in experimental glaucoma. METHODS. Ocular hypertension was induced in BrownNorway rats by injection of hypertonic saline into an episcleral vein. Retinas were processed for simultaneous visualization of the retinal microvasculature and RGCs in glaucomatous and control eyes. Retinal blood flow was examined by quantitative autoradiography using N-isopropyl-p-[14 C]-iodoamphetamine. Vascular reactivity was further assessed using an in vitro retinal microvasculature preparation.RESULTS. Substantial loss of retinal capillaries was observed after induction of ocular hypertension. The onset of both microvasculature and RGC loss occurred early and proceeded at a similar rate for at least 5 weeks after the initial damage. Systemic administration of galantamine preserved microvasculature density and improved retinal blood flow in glaucomatous retinas. The vasoactive effects of galantamine on retinal microvessels occurred through activation of muscarinic acetylcholine receptors both in vitro and in vivo.CONCLUSIONS. The onset and progression of microvessel and RGC loss are concomitant in experimental glaucoma, suggesting a tight codependence between these cellular compartments. Early interventions aimed to protect the retinal microvasculature and improve blood supply are likely to be beneficial for the treatment of glaucoma.

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Changes in the oscillatory potentials of the electroretinogram in glaucoma

Cited by 43 publications

References 12 publications

Characterization of retinal damage in the episcleral vein cauterization rat glaucoma model

Characterization of retinal damage in the episcleral vein cauterization rat glaucoma model

Electroretinographic Abnormalities in a Rat Glaucoma Model with Chronic Elevated Intraocular Pressure

Acetylcholinesterase Inhibition Promotes Retinal Vasoprotection and Increases Ocular Blood Flow in Experimental Glaucoma

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