Identifying Cell Class Specific Losses from Serially Generated Electroretinogram Components

PURPOSE Processing of information through the cellular layers of the retina occurs in a serial manner. In the electroretinogram (ERG), this complicates interpretation of inner retinal changes as dysfunction may arise from "upstream" neurons or may indicate a direct loss to that neural generator. We propose an approach that addresses this issue by defining ERG gain relationships. METHODS Regression analyses between two serial ERG parameters in a control cohort of rats are used to define gain relationships. These gains are then applied to two models of retinal disease. RESULTS The PIII(amp) to PII(amp) gain is unity whereas the PII(amp) to pSTR(amp) and PII(amp) to nSTR(amp) gains are greater than unity, indicating "amplification" (P < 0.05). Timing relationships show amplification between PIII(it) to PII(it) and compression for PII(it) to pSTR(it) and PII(it) to nSTR(it), (P < 0.05). Application of these gains to ω-3-deficiency indicates that all timing changes are downstream of photoreceptor changes, but a direct pSTR amplitude loss occurs (P < 0.05). Application to diabetes indicates widespread inner retinal dysfunction which cannot be attributed to outer retinal changes (P < 0.05). CONCLUSIONS This simple approach aids in the interpretation of inner retinal ERG changes by taking into account gain characteristics found between successive ERG components of normal animals.