April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Mice With Thinner Corneas Show Altered Retinal Function and Response to Intraocular Pressure Challenge
B. V. Bui; Y. Kong; J. Craig; D. P. Dimasi; R. Savarirayan; D. A. Mackey; K. Burdon
Author Affiliations & Notes
  • B. V. Bui
    Optometry and Vision Sciences,
    University of Melbourne, Parkville, VIC, Australia
  • Y. Kong
    Glaucoma Research Unit, Centre for Eye Research Australia, East Melbourne, VIC, Australia
  • J. Craig
    Department of Ophthalmology, Flinders University, Bedford Park, SA, Australia
  • D. P. Dimasi
    Department of Ophthalmology, Flinders University, Bedford Park, SA, Australia
  • R. Savarirayan
    Peadiatrics Royal Children's Hospital,
    University of Melbourne, Parkville, VIC, Australia
  • D. A. Mackey
    Lions Eye Inst/Uni of Western Australia, Nedlands, WA, Australia
  • K. Burdon
    Department of Ophthalmology, Flinders University, Bedford Park, SA, Australia
  • Footnotes
    Commercial Relationships  B.V. Bui, None; Y. Kong, None; J. Craig, None; D.P. Dimasi, None; R. Savarirayan, None; D.A. Mackey, None; K. Burdon, None.
  • Footnotes
    Support  NHMRC 537077, NHMRC 566570 (BV Bui)
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 6394. doi:
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      B. V. Bui, Y. Kong, J. Craig, D. P. Dimasi, R. Savarirayan, D. A. Mackey, K. Burdon; Mice With Thinner Corneas Show Altered Retinal Function and Response to Intraocular Pressure Challenge. Invest. Ophthalmol. Vis. Sci. 2010;51(13):6394.

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Abstract

Purpose: : Thinner corneas have been identified as a risk factor for glaucoma. B6C3Fe a/a-Col1a2oim/J mice have a single base pair deletion in the Col1A2 gene. Dominant mutations to Col1A2 cause Osteogenesis Imperfecta (OI), a condition associated with thin central corneal thickness (CCT). Col1A2 homozygous mice have mild skeletal abnormalities akin to human OI, and thinner CCT (74.4 ± 7.3 vs 87.7 ± 9.3 um). We consider whether eyes of Col1A2 mice on C57Bl6 background are more susceptible to intraocular pressure (IOP) challenge than wildtype animals.

Methods: : Retinal function was assessed using the electroretinogram (ERG) at baseline (n=10/group), during (30 min, homozygous Col1A2n=8, wildtype n=14) and after IOP challenge (90 min) in anaesthetized (70:7 mg/kg, ketamine:xylazine, 30% top up/30 min) dark-adapted mice. One eye was assigned to IOP challenge (50 mmHg) the other remained at baseline (15 mmHg). ERGs were analyzed for the major components, and expressed as percentage change (mean ±SEM).

Results: : Compared to wildtype animals, Col1A2 mice showed normal phototransduction amplitude (-1 ± 9%) and sensitivity (p>0.05). Responses arising from the cone pathway (cone-P2 +23 ± 11, rod-P2 +4 ± 8%) were larger and faster (cone-P2 -6.9 ± 0.9, rod-P2 -13.4 ± 0.7 ms). Oscillatory potentials were enhanced (cone-OP +29 ± 14, rod-OP +74 ± 15%). Rod OPs were faster (-3.9 ± 0.5 ms), whereas cone OPs were slower (+11.6 ± 3.6 ms). The positive lobe of the ganglion cell scotopic threshold response was larger (pSTR +75 ± 27%) the negative lobe was smaller (nSTR -23 ± 15%), both were faster (pSTR -22.7 ± 2.6, nSTR -26.7 ± 2.9 ms). During IOP challenge Col1A2 eyes showed significantly greater pSTR (Col1A2 -64 ± 8 vs wildtype -37 ± 14%, p < 0.01) and nSTR loss (Col1A2 -62 ± 13 vs wildtype -48 ± 10%, p < 0.05). The onset of nSTR loss was faster in Col1A2 eyes. pSTR (p = 0.02) and nSTR (p = 0.03) recovery after IOP-challenge was slower in Col1A2 compared with wildtype mice. P2 amplitudes were similarly affected in Col1A2 and wildtype animals during (p = 0.13) and after (p = 0.52) IOP challenge.

Conclusions: : In response to IOP-challenge Col1A2 eyes showed greater dysfunction and slower recovery. These data suggest that abnormalities in structural collagen can modify the eyes response to IOP challenge.

Keywords: electroretinography: non-clinical • intraocular pressure • ganglion cells 
© 2010, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.
Copyright © 2024 Association for Research in Vision and Ophthalmology.
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