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The homozygous parent strain of the P23H transgenic rat (developed as an animal model or retinal degeneration associated with human eye disease) was crossed with pigmented wild-type (Long Evans) rats. The pigmented offspring, heterozygous for the mutation in the rhodopsin gene, more closely resemble the human disease state. Single and paired-flash electroretinography was used to evaluate the retinal response to brief light flashes. A-wave amplitudes and sensitivity decreased with age up to 12 wks (the oldest rats currently in the colony); b-wave amplitudes and sensitivity were relatively preserved up to 12 wks. At 4 wks of age, the transgenic rats showed an earlier time to peak of the paired-flash-derived photoreceptor response, and a faster initial recovery from peak, when compared to age-matched wild-type.