June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Anti-Diuretic Hormone in the Regulation of Ocular Volume in Compensation to Defocus
Author Affiliations & Notes
  • Melanie Murphy
    Psychological Science, La Trobe University, Melbourne, VIC, Australia
  • Loretta Giummarra
    Psychological Science, La Trobe University, Melbourne, VIC, Australia
  • Nina Riddell
    Psychological Science, La Trobe University, Melbourne, VIC, Australia
  • David P Crewther
    Centre for Human Psychopharmacology, Swinburne University of Technology, Melbourne, VIC, Australia
  • Vinh Nguyen
    Psychological Science, La Trobe University, Melbourne, VIC, Australia
  • Sheila Gillard Crewther
    Psychological Science, La Trobe University, Melbourne, VIC, Australia
  • Footnotes
    Commercial Relationships Melanie Murphy, None; Loretta Giummarra, None; Nina Riddell, None; David Crewther, None; Vinh Nguyen, None; Sheila Crewther, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2165. doi:
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      Melanie Murphy, Loretta Giummarra, Nina Riddell, David P Crewther, Vinh Nguyen, Sheila Gillard Crewther; Anti-Diuretic Hormone in the Regulation of Ocular Volume in Compensation to Defocus. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2165.

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

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Abstract

Purpose: The hormone Arginine Vasopressin (AVP) is a vasoconstrictor and anti-diuretic that is commonly associated with stress. Our previous results show that AVP causes a myopic shift in refractive compensation (RC) to +10D defocus (ARVO, 2013). Further, environmental stress in the form of asymmetric flicker impacts ocular growth (Crewther et al, 2006). Thus the current experiment aimed to investigate whether AVP plays a role in RC to defocus, and whether flicker affects this process.

Methods: Experiment 1: RNA was extracted from the retina/RPE/choroid of chicks with + or -10D, or no defocus on days 5-7 post-hatching (n = 3 per lens group, per day) and prepared for sequencing on the Illumina HiSeq1500. Raw reads were mapped onto the chick genome and counts determined for each gene. Counts per million were imported into Pathway studio and GSEA conducted using the Mann-Whitney U-test algorithm (p<.05).<br /> Experiment 2: Chicks (n=360) were raised from day 5-9, with or without asymmetric flicker in the 12 hr day cycle, with + or -10D defocus (or non lens), following intravitreal injection of 5µl of either PBS, AVP or the AVP receptor antagonist ([des-Gly9-β-Mercapto-β, β cyclopentamethylenepropionyl1, O-Et-Tyr2,Val4,Arg8]-Vasopressin) (in PBS) into the experimental eye. Fellow eyes were injected with PBS. Retinoscopy and A-scan ultrasonography was performed on day 9. Tissue was collected and prepared for immunohistochemistry to examine AQP-4 and Kir4.1 expression.

Results: Experiment 1: RNAseq revealed sign-dependent changes in AVP-related pathways over 3 days of rearing with defocus.<br /> Experiment 2: Flicker alone induced a myopic shift in both lens conditions. Flicker+AVP reduced hyperopia, axial elongation and anterior chamber depth in +10D lenses. Flicker+AVP antagonist reduced RC and ocular growth to -10D lenses. Immunohistochemistry showed altered AQP-4 and Kir4.1 staining across flicker conditions.

Conclusions: Results indicate that changes in AVP-related gene expression occur concomitantly with changes in ocular volume during the induction of RC. Further, AVP and its antagonist also differentially interfered with the typical pattern of compensation to lenswear. Physiological stress induced by flickering light further influenced this. These results implicate stress-induced changes in the rate of transretinal fluid movement in the development of refractive error.

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