September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
NBCe1A (Slc4a4A) knockout causes retinal thinning and reduced ERG activity
Author Affiliations & Notes
  • Chelsea Carlson
    Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
  • Heather Holmes
    Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
  • Adam Rossano
    Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
    Nephrology & Hypertension, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
  • An-Ping Chen
    Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
  • Min-Hwang Chang
    Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
  • Michael F Romero
    Physiology & Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
    Nephrology & Hypertension, Mayo Clinic College of Medicine, Rochester, Minnesota, United States
  • Footnotes
    Commercial Relationships   Chelsea Carlson, None; Heather Holmes, None; Adam Rossano, None; An-Ping Chen, None; Min-Hwang Chang, None; Michael Romero, None
  • Footnotes
    Support  EY17732, EY21727, Mayo PREP program (R25 GM075148), Kogod Aging Center, Mayo Foundation
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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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)

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Abstract

Purpose : 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.

Methods : 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.

Results : 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.

Conclusions : 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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