Table of Contents Author Guidelines Submit a Manuscript
Journal of Ophthalmology
Volume 2011, Article ID 507037, 6 pages
http://dx.doi.org/10.1155/2011/507037
Review Article

Cellular Origin of Spontaneous Ganglion Cell Spike Activity in Animal Models of Retinitis Pigmentosa

1Program in Neurobiology and Behavior, Department of Physiology and Biophysics, University of Washington, Seattle, WA 98195, USA
2Department of Neurophysiology, Brain Research Institute, University of Zurich, 8057 Zurich, Switzerland

Received 1 July 2010; Accepted 7 September 2010

Academic Editor: Ian M. MacDonald

Copyright © 2011 David J. Margolis and Peter B. Detwiler. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Here we review evidence that loss of photoreceptors due to degenerative retinal disease causes an increase in the rate of spontaneous ganglion spike discharge. Information about persistent spike activity is important since it is expected to add noise to the communication between the eye and the brain and thus impact the design and effective use of retinal prosthetics for restoring visual function in patients blinded by disease. Patch-clamp recordings from identified types of ON and OFF retinal ganglion cells in the adult (36–210 d old) rd1 mouse show that the ongoing oscillatory spike activity in both cell types is driven by strong rhythmic synaptic input from presynaptic neurons that is blocked by CNQX. The recurrent synaptic activity may arise in a negative feedback loop between a bipolar cell and an amacrine cell that exhibits resonant behavior and oscillations in membrane potential when the normal balance between excitation and inhibition is disrupted by the absence of photoreceptor input.