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S. Viswanathan, A.J. Weber, C.D. Harman; Retinal Ganglion Cell Component of the Full–Field Photopic Flash Electroretinogram Revealed by Optic Nerve Damage in the Cat . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4731.
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The photopic flash electroretinogram (ERG) of the cat contains negative potentials – the Photopic Negative Response (PhNR), following light onset and offset that depend on spiking activity of inner–retinal neurons. The present study examined the relative contribution of retinal ganglion cells (RGCs) to these negative potentials in the cat.
Full–field photopic flash ERGs were recorded from adult cats under ketamine/xylazine that had either retrograde degeneration of RGCs at 1 week after severe optic nerve crush or suppression of spiking activity of inner–retinal neurons with intravitreal application of tetrodotoxin (TTX). Test stimuli were 750 ms red flashes (1 to 75 ph cd/m2) delivered on a constant rod–saturating blue background (75 sc cd/m2). Animals were sacrificed on recovery from anesthesia and RGC counts were made from flat mount retinas.
ERG from control eyes contained transient negative potentials after both stimulus onset and offset. Amplitude of the negative potentials increased with test flash intensity and their implicit time reduced from 150 ms at lower intensities to about 120 and 90 ms after stimulus onset and offset respectively at higher intensities. TTX greatly reduced the negative potentials at all intensities. ERGs from eyes with nerve crush (showing 50% RGC loss at 1 week) demonstrated loss of only a slow negative component following both light onset and offset that had implicit times around 150 ms. While the slow potentials removed in eyes with nerve crush dominated the overall ERG response at the lower flash intensities and had time course similar to the response removed by TTX, they constituted only a smaller proportion of the overall negative potentials removed by TTX at higher intensities.
Our data indicate that while negative potentials in the photopic flash ERG of the cat depend on spiking activity of inner–retinal neurons, RGC contributions to these potentials are mainly of the form of a slow negative component. Longitudinal studies are underway to determine the alterations resulting from further loss of RGCs.
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