Theodore G. Drivas, Jean Bennett  Neuron 

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The Bionic Retina: A Small Molecule with Big Potential for Visual Restoration  Theodore G. Drivas, Jean Bennett  Neuron  Volume 75, Issue 2, Pages 185-187 (July 2012) DOI: 10.1016/j.neuron.2012.06.010 Copyright © 2012 Elsevier Inc. Terms and Conditions

Figure 1 The Bionic Retina (A) Architecture of a normal versus a degenerated retina. The latter lacks both rod and cone photoreceptors. In the wild-type retina, incident light penetrates through the layers of the retina and is absorbed by the photoreceptor outer segments, where it is converted to an electrical signal (straight red arrow). The signal is propagated through and modified by the inner retinal neurons and eventually integrated by the ganglion cells before being passed to the brain via the optic nerve. Since photoreceptors are absent in the degenerated retina, there is no electrical response to illumination. (B) The mechanism of action of AAQ, a small-molecule photoactivatable K+ channel inhibiter, is represented schematically at the top. Intravitreal injection of AAQ in retinal degeneration mice results in light-dependent activation of the remaining amacrine, bipolar and ganglion cells, and output of electrical signals to the brain. (C) Some of the many methods currently being developed as therapies for retinal degeneration. Each diagram shows the light-activatable cell type or device (red hatches) and the pathway of the light-generated electrical activity (straight red arrows) from the retina to the brain. More detailed discussion of each of these strategies can be found in the text of this article. Illustration is by Mary Leonard, Biomedical Art & Design. Neuron 2012 75, 185-187DOI: (10.1016/j.neuron.2012.06.010) Copyright © 2012 Elsevier Inc. Terms and Conditions