Abstract
Purpose: :
Aquaporins (AQP) are transmembrane proteins that function as water channels across cell membranes. In the neural retina, AQP4 is found on Muller cells and has been postulated to play a role in rapid cellular water movements accompanying light–dark transduction (Verkman, 2003). As we have previously shown (ARVO 2005) that AQP4 expression is associated with the development of form deprivation myopia we now predict that AQP4 will be differentially expressed during the optical induction of myopia and hyperopia.
Methods: :
Thirty chickens were raised from day 5 with monocular +/–10D spectacle goggles which were removed after various times (t=24, 48, 72, 96 or 120 hours) of visual experience. Retinoscopy to determine refractive error and ultrasonography for axial length were performed prior to sacrifice. Eyes were cryosectioned to produce transverse sections of retina, choroid and sclera for immunohistochemistry using rabbit anti–rat polyclonal AQP4 primary antibodies and fluorescent anti–IgG secondary antibodies.
Results: :
All eyes with lenses developed myopia and hyperopia. Immunohistochemistry on frozen retinal sections revealed enhanced expression of AQP4 at the ganglion cell layer and inner plexiform layer as early as 24 hours after optical defocus was initiated, when differential refractive errors were already present. Hyperopic defocus induced enhanced expression of AQP4 channels at the vitread and inner plexiform layer as the myopic refractive error increased between 24 –120 hours when compared to fellow eyes.
Conclusions: :
These results suggest that the AQP4 channels on Muller cells which function to regulate water permeability bidirectionally across the retina, are likely to be involved in the choroidal and vitreal volume changes, as seen during the induction of myopia and hyperopia.
Keywords: refractive error development • Muller cells • ion channels