| To investigate the properties of voltage-activated sodium and potassium currents of RCS rat retinal ganglion cells during retinal degeneration, and to study the synaptic connections between ganglion cells and bipolar cells.
METHODS
1. Retinal dystrophic RCS rats and non-dystrophic RCS rats aged postnatal 21 days (P21d) and P60d were used for this study. The retinal slices were prepared and whole-cell recording was adopted. The voltage-activated sodium and potassium currents were recorded applying channel blocker under voltage clamp mode. Amplitude, density of sodium and potassium currents, I-V curves and the relationship with action potential were analyzed at different postnatal stages.
2. Immunohistochemistry staining with PKCα and synaptophysin was used to study the synaptic connections and morphological properties in inner plexiform layer (INL).
RESULTS
1. Transient firing and sustained firing of RGCs in response to depolarizing currents were recorded. There were no significant differences of current amplitude and density of RGCs between retinal dystrophic (N=22 RGCs) and normal (N=16 RGCs) RCS rats at P21d. However at late stage of retina degeneration action potential could be evoked in part of RGCs（12/18）retinal dystrophic RCS rats at P60d, and the amplitude and density of sodium currents decreased dramaticly. No significant changes in potassium currents. No sodium currents and reduced potassium currents were displayed in RGCs without firing.
2. The synaptic connections could be seen clearly between ganglion cells and bipolar cells and the structure of INL was intact at P21d. The synaptic connection in INL became disordered and structural remodeling appeared.
CONCLUSION
1. Action potential could not be evoked in part of RGCs and the kinetic characteristic of sodium channel changed dramaticly at late stage of retinal degeneration. Sodium currents amplitude and density decreased significantly and I-V curve changed, suggesting that the voltage-dependent sodium channel protein of RGCs degenerated at late stage of retinal degeneration. Potassium channels appeared involved more moderate, but also impaired at late stage of retinal degeneation.
2. At late stage of retinal degeneration the structure of INL became disordered and synaptic connections remodeled, which may be one of causes impairing the kinetic characteristic of ion channels of RGCs.
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