The mouse ERG before and after light damage is independent of p53

Death of retinal photoreceptors by apoptosis is observed under many physiol ogical and pathological conditions such as histogenesis, retinal dystrophie s and light-induced photoreceptor degeneration. To date, little is known ab out regulatory mechanisms for apoptosis in the retina. The tumor suppressor gene p53 is a regulator of apoptosis in a number of systems, however, p53- independent apoptosis has also been described. We have therefore investigat ed whether the lack of p53 influences the dark-adapted ERG in C57BL/6 p53(- /-) mice compared to p53(+/+) control littermates under physiological (regu lar light-dark cycle) conditions. We also recorded ERGs at 12 to 14 h in da rkness following diffuse bright light exposure to 8'000 or 15'000 lux for 2 h. ERG analysis over a range of 6 logarithmic units of light intensity rev ealed normal and virtually identical a-, b-, c-waves and oscillatory potent ials in dark-adapted p53(+/+) and p53(-/-) mice. After exposure to diffuse white fluorescent light strong decreases of all ERG components were found t o be very similar in both genotypes. These data support the notion that the p53 protein is neither essential for normal retinal function nor for proce sses involved in light-induced depression of the ERG in mice.