May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Dynamics of Retinal Ganglion Cell Response to Challenging Visual Stimuli as Measured by Pattern Electroretinogram
Author Affiliations & Notes
  • N.M. Sorokac
    Bascom Palmer Eye Institute,
    University of Miami School of Medicine, Miami, FL
  • W.J. Buchser
    Neuroscience Program,
    University of Miami School of Medicine, Miami, FL
  • V. Porciatti
    Bascom Palmer Eye Institute,
    University of Miami School of Medicine, Miami, FL
  • Footnotes
    Commercial Relationships  N.M. Sorokac, None; W.J. Buchser, None; V. Porciatti, None.
  • Footnotes
    Support  NIH RO1 EY14957, The Glaucoma Foundation, Fight for Sight, RPB, NIH P30–EY01481
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 3749. doi:
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      N.M. Sorokac, W.J. Buchser, V. Porciatti; Dynamics of Retinal Ganglion Cell Response to Challenging Visual Stimuli as Measured by Pattern Electroretinogram . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3749.

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

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Abstract

Abstract: : Purpose: To study the autoregulation of Retinal Ganglion Cell (RGC) activity over time, as measured by the Pattern Electroretinogram (PERG), when the retina is challenged with a stimulus that maximizes PERG amplitude (Vision Res 1992;32:1199–209) and optic nerve head blood flow (ARVO abstract # 3314 2002). Methods: The PERG was recorded simultaneously from both eyes of 14 normal subjects in response to reversing horizontal gratings (16.28 /s, 1.6 cycles/degree, 25 deg field size) presented for 4 minutes. Contrast and luminance were independently changed. PERGs were sampled every 15 seconds, and their amplitude and phase were evaluated by Discrete Fourier Transform. PERG amplitude changes over time were fitted with an exponential decay function. Results: In all subjects, the PERG in response to sustained presentation of 99% contrast stimulus slowly decreased in amplitude to reach a plateau lower than the initial amplitude by 30% on average after about 2 minutes (habituation). As contrast decreased, initial amplitude decreased, the amount of habituation decreased, the time to reach plateau decreased, and phase advanced. There was no habituation for stimuli of 25% contrast or lower. Reducing the luminance of 99% contrast stimuli by 1.5 log units caused a phase delay of 6 ms and an average reduction of amplitude, but the amount of habituation remained at maximal level of about 30%. Conclusions: The contrast–dependent habituation of PERG amplitude suggests that the metabolic demand of maximally active RGCs may not be met by the available energy supply under physiological conditions. According to this model, initial amplitude represents an index of RGC activity and plateau amplitude represents a dynamic equilibrium between RGC activity and the available energy supply. The time constant of PERG amplitude habituation is longer than the optic nerve blood flow upregulation (>100 seconds vs. ∼10 seconds) in response to comparable visual stimuli (Magn Reson Med 1996;35:143–8). This time difference between PERG habituation and blood flow upregulation may reflect a relatively slow metabolic processing of the vascular–neural connection. Our results are relevant for glaucoma where both neural and vascular factors are known to cause damage to the optic nerve.

Keywords: ganglion cells • metabolism • electroretinography: non-clinical 
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