PURPOSE: Ischemia is a risk factor for eye diseases like ocular vein occlusion or glaucoma. To investigate effects of ischemia-reperfusion (I/R) a lot of different animal models are used, studying one or two different cell types, which creates heterogeneity of data. The aim of this study was to investigate the function and morphology of the whole retina and different retinal cell types in an I/R model. METHODS: I/R was induced by elevating the intraocular pressure in the right eyes of rats. Twenty-one days after ischemia, electroretinogram measurements were performed. Changes in layer thickness were investigated. Changes of RGC, amacrine-, rod bipolar-, and glia cells as well as presence of apoptosis were analyzed immunohistologically. RESULTS: A-wave- and b-wave amplitudes were decreased; histology showed a reduction of RGC- and inner plexiform layer thickness and a 29% loss of RGCs occurred in ischemic eyes (P = 0.016). An increase of apoptotic cells was detected in the GCL and INL of ischemic retinas (P < 0.05). Also, a loss of cholinergic amacrine cells (control: 11 ± 1 cells/mm, I/R: 4 ± 1 cells/mm, P < 0.001), but no change in rod bipolar cell numbers was noted. CONCLUSIONS: Our study allowed a comparison of the effects of I/R for different retinal cell types. Cells in the outer retina seemed to be more resistant to ischemic damage compared with cells of the inner retina. We hypothesize that a degenerative process, like a secondary wave of apoptosis, occurs 21 days after I/R, causing progressive damage in the retina.
PURPOSE:Ischemia is a risk factor for eye diseases like ocular vein occlusion or glaucoma. To investigate effects of ischemia-reperfusion (I/R) a lot of different animal models are used, studying one or two different cell types, which creates heterogeneity of data. The aim of this study was to investigate the function and morphology of the whole retina and different retinal cell types in an I/R model. METHODS: I/R was induced by elevating the intraocular pressure in the right eyes of rats. Twenty-one days after ischemia, electroretinogram measurements were performed. Changes in layer thickness were investigated. Changes of RGC, amacrine-, rod bipolar-, and glia cells as well as presence of apoptosis were analyzed immunohistologically. RESULTS: A-wave- and b-wave amplitudes were decreased; histology showed a reduction of RGC- and inner plexiform layer thickness and a 29% loss of RGCs occurred in ischemic eyes (P = 0.016). An increase of apoptotic cells was detected in the GCL and INL of ischemic retinas (P < 0.05). Also, a loss of cholinergic amacrine cells (control: 11 ± 1 cells/mm, I/R: 4 ± 1 cells/mm, P < 0.001), but no change in rod bipolar cell numbers was noted. CONCLUSIONS: Our study allowed a comparison of the effects of I/R for different retinal cell types. Cells in the outer retina seemed to be more resistant to ischemic damage compared with cells of the inner retina. We hypothesize that a degenerative process, like a secondary wave of apoptosis, occurs 21 days after I/R, causing progressive damage in the retina.
Authors: Diogo S Zanoni; Germana A Da Silva; Raaya Ezra-Elia; Márcio Carvalho; Juliany G Quitzan; Ron Ofri; José L Laus; Renee Laufer-Amorim Journal: Int J Exp Pathol Date: 2017-06 Impact factor: 1.925
Authors: Sandra Kuehn; Cara Rodust; Gesa Stute; Pia Grotegut; Wilhelm Meißner; Sabrina Reinehr; H Burkhard Dick; Stephanie C Joachim Journal: J Mol Neurosci Date: 2017-09-29 Impact factor: 3.444
Authors: Bailey G Hannon; Andrew J Feola; Brandon G Gerberich; A Thomas Read; Mark R Prausnitz; C Ross Ethier; Machelle T Pardue Journal: Exp Eye Res Date: 2020-11-07 Impact factor: 3.770