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Chelsea Carlson, Heather Holmes, Adam Rossano, An-Ping Chen, Min-Hwang Chang, Michael F Romero; NBCe1A (Slc4a4A) knockout causes retinal thinning and reduced ERG activity. Invest. Ophthalmol. Vis. Sci. 201657(12):.
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© ARVO (1962-2015); The Authors (2016-present)
Recessive human mutations in the electrogenic Na+/bicarbonate cotransporter-1 (NBCe1; SLC4A4; MIM#603345) cause bilateral cataracts and glaucoma, whereas an NBCe1A-isoform specific mutation (Q29X-NBCe1) causes only glaucoma. We generated A-isoform-specific (nbce1A) knockout mice and reported that these animals have elevated intraocular pressure (Romero et al, IVOS 55:2415a, 2014). In this study, we assessed ocular morphology and retinal function in nbce1A genotypes as these mice age.
Intraocular pressure (IOP) was measured with a rebound tonometer (iCare). The thickness of the cornea, anterior chamber, and retina were measured by optical coherence tomography (OCT; Phoenix Research Systems). Retinal cell activity was assessed in 19-27 month old mice using focal electroretinogram (fERG) to quantify a-waves, b-waves, and oscillatory potentials in response to multiple light intensities and these parameters were compared across genotypes.
IOP increased in nbce1A(-/-)and nbce1A(+/-) mice compared to age matched controls (+/+). OCT revealed that nbce1A(-/-) mice had smaller anterior chambers and decreased retinal thickness. There was no significant difference in corneal thickness between genotypes. ERG recordings showed that nbce1A(-/-) animals have smaller a- and b-wave amplitudes than the (+/+) or (+/-) mice.
nbce1A(-/-) mice have elevated IOP, retinal thinning, and decreased ERG activity compared to their wild-type (+/+) littermates. Together, these results indicate that nbce1A(-/-) mice may be a reasonable model to study ocular hypertension and glaucoma.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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