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Melanie J. Murphy, Jude Jayasuriya, Loretta C. Giummarra, Sheila G. Crewther; Exploring Cell Energetics in Refractive State and Ocular Volume Regulation. Invest. Ophthalmol. Vis. Sci. 2012;53(14):3453.
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© ARVO (1962-2015); The Authors (2016-present)
The mechanisms regulating the cell energetics pathways engaged to enable the rapid adjustment of ocular volume in response to optical defocus or image degradation have not been well characterized, despite the obvious need to maintain energy resources required for optimal function in the metabolically active retina. Thus, the current investigation examined the effect of inhibiting two aspects of energy supply pathways (NKATPase and Purinergic) on compensation to lens-induced defocus (LID) and form deprivation myopia (FDM).
Chicks were raised for either 5 days with +10D or -10D LID after injection of Suramin (Purinergic) or Ouabain (NKATPase), or raised for 9 days with occluders to induce FDM under a 12/12 day/night cycle. Refractive compensation at 5 days, and recovery from FDM was assessed at 0, 6 and 24 hours post-occluder removal via retinoscopy and ultrasonography. Immunohistochemical analysis assessed changes in P2X7 and P2Y6 receptor expression based on genes identified as being altered following FDM by microarray (Affymatrix) analysis (Pathway Studios, Ariadne Genomics Inc.).
Eyes injected with Ouabain to inhibit the NKATPase receptor showed reduced compensation to LID in both defocus groups and slight ocular elongation. Suramin, a purinergic receptor antagonist, differentially effected compensation and ocular growth to LID by allowing some compensation to positive defocus. Eyes with FDM showed a rapid decline in the degree of myopia, and a reduction in ocular volume over time. Alterations in P2X7 and P2Y6 receptor expression were observed in the nerve fibre layer, sublamina A and B of the inner nuclear layer and the outer retina.
Changes in purinergic receptor expression in association with drug inhibition and alterations in ocular volume following refractive compensation or recovery from FDM highlight the involvement of mechanisms typically associated with the regulation of, and adaptation to, physiological stress. These results illustrate that energy mechanisms of the retina may be redirected towards facilitating the rapid growth response to defocus, which may have consequences for more severe ocular pathologies.
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