May 2003
Volume 44, Issue 13
ARVO Annual Meeting Abstract  |   May 2003
Two Models of Experimental Myopia in the Mouse
Author Affiliations & Notes
  • R.W. Beuerman
    Singapore Eye Research Institute, Singapore, LSU Eye Center, New Orleans, LA, United States
  • A. Barathi
    Singapore Eye Research Institute, Singapore,
  • S.R. Weon
    Singapore Eye Research Institute, Singapore,
  • D. Tan
    Singapore Eye Research Institute, National University of Singapore, Singapore,
  • Footnotes
    Commercial Relationships  R.W. Beuerman, None; A. Barathi, None; S.R. Weon, None; D. Tan, None.
  • Footnotes
    Support  NMRC
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 4338. doi:
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      R.W. Beuerman, A. Barathi, S.R. Weon, D. Tan; Two Models of Experimental Myopia in the Mouse . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4338.

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

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Abstract: : Purpose: The purpose of this study was to determine the response of the mouse eye to experimental procedures for the induction of myopia and to determine if the biology of the scleral fibroblasts is changed in the process. Methods: Experiment 1: Experimental myopia was induced in 180 Balb/CJ mice by lid-suture on right eyes; left eyes were used as controls. Sclera from 30 experimental and 30 control eyes was cultured and scleral fibroblasts between passages 4-6 were used. Scleral fibroblasts were treated with atropine at concentrations of 0.1, 1, 10, and 100 µM, and DNA synthesis was determined by measuring BrdU with an ELISA procedure. Experiment 2: Minus power (-10 D) contact lenses were glued over the right eyes of 40 mice. Refraction was determined by streak retinoscopy and axial length was measured by a digital caliper. Paraffin embedded tissue was used to quantify scleral thickness. Results: Experiment 1: At 4 weeks, the axial length of the sutured eyes was significantly greater than that of the contralateral controls (3.01 ± 0.006 mm vs 2.964 ± 0.014 mm, respectively; p<0.05; n = 30), and the disparity in growth persisted at both 6 weeks (3.285 ± 0.005 mm vs 3.018 ± 0.008 mm; p<0.05; n = 60) and 8 weeks (3.839 ± 0.006 mm vs 3.453 ± 0.005 mm; p<0.01; n=90). Eight weeks after surgery, refractions were +7 to +8 D in the sutured eyes and +12 to +15 D in the control eyes. Refractions in naïve controls were greater than +15 D. BrdU incorporation was more strongly inhibited in a dose-dependent manner by atropine in the scleral fibroblasts from the controls, compared with the sutured eyes (p<0.05). Experiment 2: After 8 weeks of contact lens wear, axial length was 3.758 ± 0.002 mm; eyes without contact lenses (controls) had a mean axial length of 3.462 ± 0.004 mm (p< 0.05; n = 40). Refraction was -2 to -4 D in the lens-wearing eyes and +6 to +8 D in the controls. In the control eyes, the scleral thickness increased from the anterior to posterior sclera (anterior, 16.7 ± 0.02 µm; equator, 41.7 ± 0.01 µm; posterior, 91.7 ± 0.03 µm). In the sutured eyes, scleral thickness was similar to the controls anteriorly (16.7 ± 0.01), but thinner at the equatorial (33.3 ± 0.01 µm) and posterior (58.3 ± 0.02 µm) locations. Conclusions: The mouse eye responds to form deprivation and minus-power lens wear by developing increased axial length and scleral thinning, and proliferation of scleral fibroblasts is decreased by muscarinic antagonists.

Keywords: myopia • refractive error development • sclera 

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