May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Origins of Oscillatory Potentials in the Photopic Flash ERG of the Mouse
Author Affiliations & Notes
  • M. Kaneko
    College of Optometry, University of Houston, Houston, TX
  • H. Maeda
    Department of Ophthalmology, Kobe University School of Medicine, Kobe, Japan
  • M. Wang
    College of Optometry, University of Houston, Houston, TX
  • W. Zhou
    College of Optometry, University of Houston, Houston, TX
  • L.J. Frishman
    College of Optometry, University of Houston, Houston, TX
  • Footnotes
    Commercial Relationships  M. Kaneko, None; H. Maeda, None; M. Wang, None; W. Zhou, None; L.J. Frishman, None.
  • Footnotes
    Support  NIH Grant EY06671 (LJF), P30 EY07551 (UHCO)
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 2257. doi:
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      M. Kaneko, H. Maeda, M. Wang, W. Zhou, L.J. Frishman; Origins of Oscillatory Potentials in the Photopic Flash ERG of the Mouse . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2257.

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

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Abstract

Abstract: : Purpose: To investigate the retinal origins of oscillatory potentials (OPs) of the photopic flash ERG of the mouse using pharmacologic blockade of inner retina and ganglion cell lesions. Methods: Ganzfeld ERGs were recorded using DTL fiber electrodes from adult C57BL/6 mice anesthetized with ketamine (56 mg/kg) and xylazine (5.6 mg/kg). Stimuli were brief xenon photostrobe flashes (1.6 to 3.6 log sc td s) on a rod–suppressing background of 2.6 log sc td. Mice were light adapted for 45 minutes before recording. The following pharmacological agents were injected intravitreally in one eye of at least 3 mice: GABA (γ–aminobutyric acid, 29 mM) to block transmission to 3rd order neurons, PDA (cis–2, 3–piperidine–dicarboxylic acid, 5.2 mM) to block transmission to hyperpolarizing 2nd order and all 3rd order neurons, TPMPA (1mM) to block GABAc receptors, TTX (tetrodotoxin, 1–2 µM) to block Na+–dependent spikes. ERGs were also recorded after ganglion cells were lesioned by optic nerve crush (ONC, 42 to 63 days post crush; n=3). OPs were extracted using bandpass filtering (50–120 Hz). The amplitude of each OP was measured from the preceding trough to the positive peak. Results: The number of OPs increased from 3 for the weakest xenon flash to 6 for the strongest flashes, and all OPs were eliminated either by injection of GABA or PDA. For the strongest stimulus, TPMPA increased the number of OPs from 6 to 7, and increased the amplitude of first 4 OPs to about 136±10.4% (mean ± sem) of control, with variable effects on amplitude and frequency of later OPs. TTX eliminated the last four OPs in the response to the strongest stimulus and reduced the first to 83±5.6% and the second to 41±2.8% of the control amplitude. ONC reduced the amplitudes of OPs 1–4 to 81±3.5% of control and 5 and 6 to 35±8.5% of control. Pharmacologic effects on early OPs were similar for responses to weaker stimuli. Conclusions: The OPs of the photopic flash ERG of the mouse originate from inner retinal amacrine and ganglion cells, and are normally modulated by GABAc receptors. The OPs past the 1st and 2nd are generated mainly by Na+–dependent spiking activity, with OPs 5 and 6 originating in large part from retinal ganglion cells.

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