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Marina Renner, Gesa Stute, Heiko Schmid, Lioba Horstmann, Burkhard Dick, Stephanie C Joachim; Optic nerve degeneration after retinal ischemia-reperfusion in a rodent model. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):22.
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It is well known, that ischemia-reperfusion (I/R) leads in functional and morphological changes of different cell types of the retina. Also, axonal or myelin damage of the optic nerve (ON) were previously observed after I/R. However, the ischemic effects on the ON are not well investigated. To gain further knowledge, we performed histological analysis of ONs after I/R.
I/R was induced by raising the intraocular pressure (IOP) in one eye of rats to 140 mmHg for 1h (n=5/group). The other eye served as control (Co). 21 days after ischemia the ONs were removed and longitudinal optic nerve sections were prepared. They were stained with H&E (structure) and LFB (myelin). Additionally, the microglial immigration (Iba1), activation of macrophages (ED1), and the macroglial response (GFAP and nestin) were analyzed using immunohistochemistry (IHC). Alteration and demyelination grade was evaluated using a scoring system. ImageJ software was used for microglia cell count and to measure GFAP+ and nestin+ area. Statistical analysis was performed using student’s t-test.
Histology showed a significant damage of the ONs of I/R eyes. Significantly more inflammatory cells infiltrated the ONs of the I/R group (Co: 0.8±0.0; I/R: 2.6±0.2; p˂0.001). Additionally, large areas of demyelination could be observed after I/R (Co: 0.8±0.1; I/R: 1.6±0.1; p˂0.001). Microglial staining confirmed these observations. Significantly more Iba1+ cells were detected in I/R ONs (Co: 8.9±0.5; I/R: 23.9±3.3; p˂0.01). Furthermore, the ED1+ cell counts revealed a significant activation of macrophages (Co: 0.1±0.1; I/R: 7.0±1.7; p˂0.01). Regarding macroglial staining, no differences could be noted in GFAP+ and nestin+ area between both groups (p>0.05).
Retinal ischemia-reperfusion is a global event. We could show that it also has an intense effect on the ON. Inflammation and demyelination of optic nerves 21 days after ischemia-reperfusion right up to dissolution of the tissue could be revealed. Strong activation of microglial cells was also noted. Thus, the axonal degeneration seems to be a result of retinal damage after I/R. The macroglial staining area showed no group differences, probably due to the grave degeneration of the optic nerve at this late point of time.
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