April 2014
Volume 55, Issue 13
ARVO Annual Meeting Abstract  |   April 2014
Loss of cholinergic amacrine cells in an ischemia-reperfusion animal model
Author Affiliations & Notes
  • Heiko Schmid
    Experimental Eye Research Institute, Knappschaftskrankenhaus, Bochum, Germany
  • Marina Renner
    Experimental Eye Research Institute, Knappschaftskrankenhaus, Bochum, Germany
  • H. Burkhard Dick
    Experimental Eye Research Institute, Knappschaftskrankenhaus, Bochum, Germany
  • Stephanie C Joachim
    Experimental Eye Research Institute, Knappschaftskrankenhaus, Bochum, Germany
  • Footnotes
    Commercial Relationships Heiko Schmid, None; Marina Renner, None; H. Burkhard Dick, None; Stephanie Joachim, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 1907. doi:
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      Heiko Schmid, Marina Renner, H. Burkhard Dick, Stephanie C Joachim; Loss of cholinergic amacrine cells in an ischemia-reperfusion animal model. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1907.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: Ocular ischemic injuries like ocular vein occlusion are huge risk factors for damage of retinal neurons and often lead to loss of vision. In the last couple of years, extensive research has been performed to avoid retinal ganglion cell (RGC) loss after an ischemic event. However, very little is known about the global effect of ischemia on different retinal neurons. The goal of this study was to investigate functional and morphological changes of different cell types of the retina after ischemia-reperfusion (I/R).

Methods: I/R was induced by raising the intraocular pressure (IOP) in one eye of rats to 140 mmHg for 1h (N=5). The other eye served as control (Co). The IOP was measured regularly. 21 days after ischemia, scotopic flash electroretinogram (ERG) measurements were performed on both eyes using intensities ranging from 0.1-25 cd*s/m2. H&E staining was used to measure the retinal layer thickness. Changes of RGC, amacrine-, rod bipolar-, and glia cells were analyzed using immunohistochemistry (IHC).

Results: No changes in IOP were noted between I/R and Co (p>0.05). The ERG measurement revealed a decrease of a-wave (p<0.01) and b-wave amplitude (p<0.001) in I/R animals at different light intensities. Histology showed a reduction of the RGC (Co: 7.1±0.4 µm, I/R: 5.8±0.2 µm, p=0.0022) and the inner plexiform layer (Co: 25.6±1.2 µm, I/R: 15.4±1.8 µm, p<0.001) thickness in I/R. No changes of the other layers were observed. IHC revealed a RGC decrease (Co: 34±2 cells/mm, I/R: 24±2 cells/mm, p=0.0016) caused by apoptosis (Co: 68.5±3.7%, I/R: 88.5±2.3%, p<0.001). A loss of cholinergic amacrine cells (Co: 11±1 cells/mm, I/R: 4±1 cells/mm, p<0.001) as well as an increase of GFAP+ area was detected in I/R (Co: 3.1±0.3, I/R: 9.4±1.4, p<0.001). Counting of rod bipolar cells stained with PKC± revealed no differences between both groups (p>0.05) and no changes in the morphology of these cells were observed.

Conclusions: We hypothesize that, although I/R is a global event, the inner retina is the primary site of damage after I/R. RGCs and amacrine cells seem to be affected first. We also assume that damage later spreads to the outer retina. We could show by a reduced b-wave amplitude that cells like rod bipolar cells, while morphologically intact, are functionally impaired. This leads us to the conclusion that only using both histology and electrophysiology gives accurate insight on the pathomechanisms of I/R.

Keywords: 572 ischemia • 435 bipolar cells • 510 electroretinography: non-clinical  

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