April 1988
Volume 29, Issue 4
Free
Articles  |   April 1988
Evidence in support of a photoreceptoral origin for the "light-peak substance".
Author Affiliations
  • R P Gallemore
    Department of Physiology, University of California, San Francisco 94143-0444.
  • E R Griff
    Department of Physiology, University of California, San Francisco 94143-0444.
  • R H Steinberg
    Department of Physiology, University of California, San Francisco 94143-0444.
Investigative Ophthalmology & Visual Science April 1988, Vol.29, 566-571. doi:
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    • Get Citation

      R P Gallemore, E R Griff, R H Steinberg; Evidence in support of a photoreceptoral origin for the "light-peak substance".. Invest. Ophthalmol. Vis. Sci. 1988;29(4):566-571.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

The light peak of the DC ERG was recorded in in vitro preparations of chick neural retina-RPE-choroid. Either the pharmacological agents Co2+, Mg2+, and low Ca2+, known to block calcium-dependent synaptic transmission or 2-amino-4-phosphonobutyric acid (APB), which blocks transmission in the ON pathway, were added to the solution perfusing the retina. These agents suppressed the b-wave of the ERG, thus indicating a severe suppression of synaptic transmission in the neural retina. The retina was also perfused with the OFF pathway inhibitor cis-2,3-piperidine dicarboxylic acid (PDA). None of these agents, however, significantly depressed the light peak, supporting the hypothesis that the light peak is generated by a photoreceptor-RPE interaction.

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