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Pharmacological studies of the mouse cone electroretinogram

Published online by Cambridge University Press:  06 December 2005

SUMIT SHARMA ,
SHERRY L. BALL  and
NEAL S. PEACHEY
SUMIT SHARMA
Affiliation:
Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland
SHERRY L. BALL
Affiliation:
Research Service, Cleveland VAMC, Cleveland Cole Eye Institute, Cleveland Clinic Foundation, Cleveland
NEAL S. PEACHEY
Affiliation:
Research Service, Cleveland VAMC, Cleveland Cole Eye Institute, Cleveland Clinic Foundation, Cleveland
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Abstract

Electroretinography provides a useful noninvasive approach to evaluate cone pathway activity. Despite wide application of the cone ERG to characterize retinal function in transgenic mice and mouse models of human hereditary retinal disease, the cellular origins of the mouse cone ERG have not been well defined. Here, we address this issue using a pharmacological approach that has been previously applied to other species. Agents that block receptor activation at well-defined retinal loci were dissolved in saline and injected into the vitreous of anesthetized adult BALBc/ByJ mice; cone ERGs were recorded 1–2 h later. Analysis of the resulting waveforms indicated that the mouse cone ERG includes a cornea-negative component that is derived from the activity of cone photoreceptors and retinal glial (Müller) cells. Similar to other species, activity of cone depolarizing bipolar cells contributes a large amplitude cornea-positive potential to the mouse cone ERG. In contrast to primate but similar to rat, the mouse cone ERG includes only a small contribution from hyperpolarizing bipolar cell activity. The inner retina appears to contribute to both the a- and b-waves of the mouse cone ERG. These results provide a foundation for interpreting changes in the waveform of the mouse cone ERG that may be observed following genetic alteration or other experimental treatment.

Keywords

ElectroretinogramBipolar cellCone photoreceptorMouse
Type
Research Article
Information
Visual Neuroscience , Volume 22 , Issue 5 , September 2005 , pp. 631 - 636
Copyright
© 2005 Cambridge University Press

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