Abstract
Currently there is no consensus regarding the aetiology of the excessive ocular volume that characterizes high myopia. Thus, we aimed to test whether the gene pathways identified by gene set enrichment analysis of RNA-seq transcriptomics refutes the predictions of the Retinal Ion Driven Efflux (RIDE) hypothesis when applied to the induction of form-deprivation myopia (FDM) and subsequent recovery (post-occluder removal). We found that the induction of profound FDM led to significant suppression in the ligand-gated chloride ion channel transport pathway via suppression of glycine, GABAA and GABAC ionotropic receptors. Post-occluder removal for short term recovery from FDM of 6 h and 24 h, induced significant upregulation of the gene families linked to cone receptor phototransduction, mitochondrial energy, and complement pathways. These findings support a model of form deprivation myopia as a Cl− ion driven adaptive fluid response to the modulation of the visual signal cascade by form deprivation that in turn affects the resultant ionic environment of the outer and inner retinal tissues, axial and vitreal elongation as predicted by the RIDE model. Occluder removal and return to normal light conditions led to return to more normal upregulation of phototransduction, slowed growth rate, refractive recovery and apparent return towards physiological homeostasis.
Highlights
There is no consensus regarding the aetiology of the excessive ocular volume that characterizes high myopia
Less refractive compensation was seen after 24 h of visual recovery post-occluder removal (− 16.4 ± 1.18D), presumably due to the circadian impact of the regular night period with this measurement being made 2 h after the first 12 h night/dark period (Fig. 1a)
The same trend was seen in vitreous chamber depth (VCD) and anterior chamber (AC) at 6 h with VCD reduced by 0.08 mm and AC by 0.04 mm indicating that the excessive ocular growth response to FD is inhibited by occluder removal and that normal light conditions favour re-emmetropisation
Summary
There is no consensus regarding the aetiology of the excessive ocular volume that characterizes high myopia. In animal models of myopia, rapid axial elongation, refractive change and altered gene expression[28] is seen following 6 h of − 10D optical defocus in chicks or within 30mins of removal of form deprivation[29]; see Fig. 1 One such physiological model of myopia development based on very well established retinal/RPE physiology and extensive literature relating to rapid light/dark induced fluid shifts in the r etina[29,30,31,32,33] has been proposed by Crewther[34] as the Retinal Ion Driven Efflux (RIDE) model of myopia. We aimed to investigate if the biochemical pathways identified by RNAseq transcriptomics during induction of FDM and short term recovery would refute or add any support for the RIDE model theory
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