May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Effects of Pharmacological Agents on the Pattern and Photopic Flash ERG of the Mouse
Author Affiliations & Notes
  • G. Miura
    Optometry, University of Houston-Downtown, Houston, Texas
  • K. M. Ivers
    Optometry, University of Houston-Downtown, Houston, Texas
  • M. Wang
    Optometry, University of Houston-Downtown, Houston, Texas
  • L. J. Frishman
    Optometry, University of Houston-Downtown, Houston, Texas
  • Footnotes
    Commercial Relationships G. Miura, None; K.M. Ivers, None; M. Wang, None; L.J. Frishman, None.
  • Footnotes
    Support NIH Grant EY06671 (LJF), P30 07551 (UHCO)
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 1292. doi:https://doi.org/
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      G. Miura, K. M. Ivers, M. Wang, L. J. Frishman; Effects of Pharmacological Agents on the Pattern and Photopic Flash ERG of the Mouse. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1292. doi: https://doi.org/.

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

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Abstract

Purpose:: To investigate the retinal origins of the pattern ERG (PERG) by using pharmacological agents in the mouse retina.

Methods:: PERGs and photopic ganzfeld ERGs (FERGs) were recorded from anesthetized C57BL/6 mice 3-4 months of age. Recordings were made before and after intravitreal injections of PDA (cis-2, 3-piperidine-dicarboxylic acid, 3-5 mM) to block transmission to hyperpolarizing 2nd order and all 3rd order neurons, TTX (tetrodotoxin, 1-2 µM) to block Na+-dependent spikes and APB (2-amino-4-phosphonobutyric acid, 1.6-2.0 µM) to block synapses between photoreceptors and ON-bipolar cells. The pattern stimuli consisted of contrast reversing gratings (1 Hz) of 0.05 cy/deg presented at various contrasts (50% to 90%). Brief green ganzfeld flashes (0.4-2.5 log sc td s) were presented on a rod suppressing green background of 2.6 log sc td.

Results:: PERGs were similar in waveform for all contrasts (but 50% where PI was delayed), with a positive peak (P1) around 61 ms and maximum negative trough (N2) around 130 ms; amplitudes were greatest for 90% contrast. For control eyes, the mean amplitude (90% contrast) of P1 was 6.0µV (SD=1.75, n=12), and the mean amplitude of the peak to trough (P1N2 at 130 ms) was 10.5 µV (SD=1.65, n=12). PDA and TTX both delayed P1, PDA by a mean of 16 ms, TTX, by 12 ms. Because the delay was even greater in N2, P1N2 was not measured. PDA reduced P1 by about 61% on average (mean amplitude, 2.70 µV, SD=0.63, n=4), while for the FERG (2.5 log sc td s), a-wave amplitudes were reduced by 48%, OPs were removed, but b-waves were hardly affected. TTX reduced P1 by about 70% (mean, 1.6 µV, SD=0.05, n=4), while FERG a-waves were increased by 43% and b-wave amplitudes were reduced by 56%. APB injections removed P1, leaving a negative wave of a different time course than N2. In the FERG, APB removed the b-wave, producing a negative ERG.

Conclusions:: PERG P1 amplitudes were greatly reduced but not eliminated by PDA which should have removed all activity of 3rd order neurons, and by TTX, which should have substantially attenuated that activity. These results together with APB results suggest that the mouse PERG P1 wave is dominated by contributions from the 3rd order neurons in the ON pathway, but includes light-evoked activity of more distal retinal neurons.

Keywords: electroretinography: non-clinical • retina • retina: proximal (bipolar, amacrine, and ganglion cells) 
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