|Blind Mice Recover Visual Responses Using Protein from Green
Nerve cells that normally are not light sensitive in the retinas of blind mice
can respond to light when a green algae protein called channelrhodopsin-2 (ChR2)
is inserted into the cell membranes, according to a National Institutes of Health
(NIH)-supported study published in the April 6, 2006 issue of the journal Neuron.
The study was conducted with mice that had been genetically bred to lose rods
and cones, the light-sensitive cells in the retina. This condition is similar
to the blinding disease retinitis pigmentosa (RP) in humans.
Vision normally begins when rods and cones, also called photoreceptors, respond
to light and send signals through the retina and the optic nerve to the visual
cortex of the brain, where visual images are formed. Unfortunately, photoreceptors
degenerate and die in some genetic diseases, such as RP. Both mice and humans
go progressively blind because with the loss of rods and cones there is no signal
sent to the brain.
This study, funded by the National Eye Institute (NEI) of the NIH, raises the
intriguing possibility that visual function might be restored by conveying light-sensitive
properties to other surviving cells in the retina after the rods and cones have
died. Principal investigator Zhuo-Hua Pan, Ph.D., of Wayne State University School
of Medicine, and his colleagues, using a gene-transfer approach, introduced the
light-absorbing protein ChR2 into the mouse retinal cells that survived after
the rods and cones had died. These cells became light sensitive and sent signals
through the optic nerve to the visual cortex.
“This innovative gene-transfer approach is certainly compelling,” said Paul
A. Sieving, M.D., Ph.D., director of vision research at the NIH. “This is a clever
approach that offers the possibility of some extent of vision restoration at
some time in the future.” In addition to RP, there are many forms of retinal
degenerative eye diseases that possibly could be treated by gene-based therapies.
The researchers determined that the signals reached the visual cortex in a majority
of the ChR2-treated mice. The light sensitivity persisted for at least six months.
Did the mice regain usable vision? Probably not, but the investigators suggest
a number of technical improvements to their experiments which might make that
“This study demonstrates the feasibility of restoring visual responses in mice
after they lose the light-sensitive photoreceptor cells,” said Dr. Pan. He and
his colleague, Alexander Dizhoor, Ph.D., of Pennsylvania College of Optometry,
another of the study authors, think that expressing ChR2 in other types of retinal
cells may help to improve this approach. In addition, the authors state it would
be interesting for further study to modify the light sensitivity and/or wavelength
selectivity of ChR2, or use similar microbial proteins, to produce diverse light-sensitive
channels to improve outcomes for the possible restoration of normal vision.
The National Eye Institute (NEI) is part of the National Institutes of Health
(NIH) and is the Federal government's lead agency for vision research that
leads to sight-saving treatments and plays a key role in reducing visual impairment
and blindness. For more information, visit the NEI Website at http://www.nei.nih.gov/.
The National Institutes of Health (NIH) — The Nation's Medical Research
Agency — includes 27 Institutes and Centers and is a component of
the U.S. Department of Health and Human Services. It is the primary federal
agency for conducting and supporting basic, clinical and translational medical
research, and it investigates the causes, treatments, and cures for both common
and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.