Purchase this article with an account.
Katherine Mancuso, Maureen Neitz, Jay Neitz; Gaining insights to the neural code for color by attempting gene therapy for color blindness. Journal of Vision 2004;4(11):65. doi: 10.1167/4.11.65.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Recent evidence from molecular genetics and developmental studies suggests that the L and M cone photoreceptors in Old World primates, including humans, exist as a single cell type until a stochastic event within each photoreceptor results in the exclusive expression of L or M pigment. Thus, there does not appear to be a mechanism to communicate the identity of L vs. M cones to the post-synaptic neurons. This evidence favors the hypothesis that during primate evolution, L/M opponent ganglion cells could have arisen by random wiring to a newly introduced mosaic of L and M cones. The ‘random wiring’ hypothesis has been a subject of debate. While it may be possible to explain how the color circuits arise at the level of the retina, one limitation of the theory is that understanding specifically how the cortical circuits for color vision might arise from random connections has been difficult. In the present work, we have developed a model which extends the random wiring theory to the cortex. It is proposed that the cortical circuits for red-green color vision arise by hijacking the preexisting blue-yellow system. This model predicts that it should be possible to cure adults who are red-green color blind through a gene therapy procedure in which a retrovirus that contains a human visual pigment gene will transduce a subset of the foveal cones and therefore produce three distinct cones types. Experiments to test this theory in an adult squirrel monkey model are underway.
This PDF is available to Subscribers Only