April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
An Experimental Mouse Model of Contusive Retinal Detachment
Author Affiliations & Notes
  • Fansheng Kong
    School of Ophthalmology and Optometry, Wenzhou Medical College, Wenzhou City, China
  • Rui Zeng
    School of Ophthalmology and Optometry, Wenzhou Medical College, Wenzhou City, China
  • Ying Zhang
    School of Ophthalmology and Optometry, Wenzhou Medical College, Wenzhou City, China
  • Fanjun Shi
    School of Ophthalmology and Optometry, Wenzhou Medical College, Wenzhou City, China
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 5343. doi:
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      Fansheng Kong, Rui Zeng, Ying Zhang, Fanjun Shi; An Experimental Mouse Model of Contusive Retinal Detachment. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5343.

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Abstract

Purpose: : To reveal an experimental mouse model of contusive retinal detachment (CRD) which was created without directly manipulating retina with mechanical or liquid means.

Methods: : Being observed under surgical microscope, a 30 1/2-gauge beveled needle was used to puncture through the cornea of C57BL/6 mice, causing transient leakage of aqueous humor, leading to the formation of retinal bleb. The apparent changes of the retinal blebs were examined via observing the fundus of live punctured eyes and eyecups made from punctured eyes at various time points post puncturing (PP). Both light microscopy and electroretinograph (ERG) were performed to assess histological, morphological and functional changes of the retina. Terminal deoxynucleotidyl transferase-mediated uridine 5’-triphosphate-biotin nick end labeling (TUNEL) technique was performed to examine internucleosomal DNA fragmentation.

Results: : A single puncturing through the cornea into the anterior chamber could immediately lead to the formation of multiple retinal blebs. The retinal blebs became shrunken and flat automatically within 24 hours PP. Observation with surgical microscope showed that there were no breaks or holes on the retina of both live and eyecup made from punctured eyes. Light microscopy demonstrated that the retinal blebs were in a formation of RD formed between the neuroretinal layer and the retina pigment epithelium (RPE) layer and the RPE cells at the site of detachment appeared apically enlarged containing a giant vacuole. At 11-13 days PP, almost all the sections of punctured eyes showed no separation between the neuroretinal layer and the RPE layer as normal mouse eyes. Relative to the contralateral none punctured eye, the punctured eyes decreased about 45% and 24% of dark-adapted b- and a-wave amplitudes respectively; and decreased about 7% and 12% of light-adapted b- and a-wave amplitudes respectively within about 10 to 20 minutes PP. At 12 hours PP, both dark- and light-adapted b- and a-wave amplitudes recovered to normal level. No TUNEL-positive cells were observed in the frozen sections of punctured eyes at various time points PP.

Conclusions: : Puncturing through a mouse cornea can lead to transient RD with no retinal breaks and holes. The ERG of the RD recovers to normal within 12 hours PP and the tissue adhesion strength of retinal reattachment following detachment reaches to almost normal level at 10-13 days PP. The RD causes no apoptosis in both RPE cell and retinal cells.The experimental mouse model of retinal detachment revealed in this study mimics contusive and exudative form of human RD or chorioretinopathy with no retinal breaks or holes.

Keywords: retinal detachment • electroretinography: non-clinical 
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