Abstract
Visually guided regulation is a sophisticated and active process, whereby sensory input helps to shape ocular development. Here, we sought to investigate the potential involvement of SorCS1, an important protein in synaptic transmission in neuron, in retinal development. A form-deprivation (FD) rat model was established. Ocular variations induced by FD were examined, including changes to eye axial length and retinal thickness. Scotopic electroretinogram (ERG) was used to examine retinal function. RD-PCR assays were screened for differentially expressed genes in FD rat eyes. Immunofluorescence staining identified the expression pattern and localization of SorCS1 in rat retina, with or without FD treatment. Additionally, primary retinal neural cells were cultured and incubated with or without a light-dark cycle, and western blot and real-time PCR assays were used to examine the expression of SorCS1. Retinal neural cells were treated with recombinant SorCS1 (h-SorCS1) coated with beads in serum-free conditions to test for effects on cellular physiology and expression of neurotransmitters involved in visual development. To monitor cell viability, a CCK8 assay was employed. Our data demonstrated that FD led to ocular axial elongation and retinal thinning. ERG tests showed FD impaired electrophysiological function in rat. An age-related expression pattern of SorCS1 was observed in the rat retina, and SorCS1 was significantly up-regulated in the FD rat retina. In addition, in vitro evidence suggested a strong correlation between light exposure and SorCS1 expression. Furthermore, treatment of retinal neural cells with h-SorCS1-beads promoted cell viability, neurite outgrowth, and up-regulation of inhibitory neurotransmitter expression, which implies that over-expression of SorCS1 may cause abnormal retinal development. Our findings suggest that SorCS1 is involved in the physiological processes of light/visually guided ocular growth.