The pirate look is a time-honored way to fix children’s “lazy eye”: the patch over the good eye forces the weak one to work, thereby preventing its deterioration. Playing video games helps, too. The neural cells corresponding to both eyes then learn to fire in synchrony so that the brain wires itself for the stereo vision required for depth perception. Left untreated past a critical age, lazy eye, or amblyopia, can result in permanently impaired vision. New studies are now showing that this condition, which affects up to 5 percent of the population, could be repaired even past the critical phase.
What is more, amblyopia may provide insights into brain plasticity that could help treat a variety of other disorders related to faulty wiring, including schizophrenia, epilepsy, autism, anxiety and addiction. These ailments “are not neurodegenerative diseases that destroy part
of the neural circuitry,” notes Takao Hensch, a Harvard Medical School researcher. So if the defective circuits “could be stimulated in the right way, the brain could develop normally.”
The recent findings have their roots in work from 10 years ago. Then, Hensch led a team that discovered the specific visual circuitry that induces a “critical period” during early life in which the two eyes must work together to establish the connections in the cortex underlying proper visual acuity. So-called parvalbumin basket cells release the neurotransmitter GABA, which puts the brakes on cell activity. But GABA and compounds that behave like it—the drug Valium, for one—can also trigger the critical phase. It is paradoxical that neurochemicals that turn cells off play a role in initiating a key developmental stage.
Hensch’s discovery, along with the recognition of the important part played by the proteins and sugars that form a matrix surrounding parvalbumin cells, has resulted in a set of recent experiments that demonstrate ways to reinstate the critical period in adult animals—and perhaps to map a path toward treatments. In 2006 a group led by Lamberto Maffei, a neurobiologist at the University of Pisa in Italy, injected an enzyme called chondroitinase into the visual cortex of adult rats with amblyopia to dissolve the extracellular matrix and restore the critical period. After patching a rat’s good eye, the researchers witnessed the recovery of normal vision: cortical circuitry for both the left and right eyes were nudged into firing together, just as they are during the early phase of childhood development.
More recently, Hensch’s team reported in Cell last summer on a protein that has the same effect as Valium in the developing visual cortex. Called Otx2, it has a role in the embryonic development of the head and becomes prominent again after birth, serving as the starting gun for the critical period. The protein actually travels from the retina to the visual cortex at the rear of the brain, perhaps because the visual cortex needs to wait for a signal from the eyes that it is ready to undergo maturation.
Hensch also presented work at the Society for Neuroscience annual meeting in November on adult mice with amblyopia that were genetically engineered to lack a receptor on neurons for Nogo, a growth-inhibiting protein that originates in the myelin insulation around the neural wires called axons. In the experiment, suturing shut one of the two healthy eyes during the critical period induced amblyopia and its attendant decrease in visual acuity. When the sutures were removed, however, the mice that did not have the molecular brake of the Nogo receptor spontaneously regained their vision.
“This work is inspirational for me,” remarks Dennis Levi, a neuroscientist at the University of California, Berkeley. “The future will be some kind of molecular intervention for amblyopia.”
Such a future may not be far off. In fact, oral compounds may already exist on the pharmaceutical shelves. Last year Maffei’s group found that the antidepressant Prozac can restore plasticity in the adult visual system of rats.
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7 Comments
Add CommentGood work. It seems that if we contron some key factors, we can reverse the development of the brain. Cool.
Reply | Report Abuse | Link to thisGood. It must be a good feeling if we can reverse the development of our brain.
Reply | Report Abuse | Link to thisI have always suffred from lack of stereo vision and wore a
Reply | Report Abuse | Link to thispatch during childhood. It is false to say that we have no 3D vision : Focussing by the lenses of the eyes create depth clues for the brain. But the image from our 'good' eye overlaps the other and deletes its overlap.
In a science park I tried 3D goggles of several different technologies. The one which sends an image to each eye alternately created the first stereo vision I have ever experienced. Oh for a permanent treatment!
Optometrists have known for decades that amblyopia can be treated at any age. Optometric vision therapy, the correct refractive prescription, patching, and atropine therapy all have a role to play. Research has shown that lazy eye is a brain problem that involves both eyes....so its treatment should involved both eyes as well. Go to http://www.covd.org and http://www.mainosmemos.blogspot.com (type in "amblyopia" in the search box) for more information
Reply | Report Abuse | Link to thisDominick M. Maino, OD, MEd, FAAO, FCOVD-A
Professor of Pediatrics/Binocular Vision Illinois College of Optometry
Interesting article - as an eye patch wearer as a child I thought that the video-games suggested as exercises could only help, just to find out that the two games mentioned are violent ones -- other ideas????
Reply | Report Abuse | Link to thisInteresting article - as an eye patch wearer as a child I thought that the video-games suggested as exercises could only help, just to find out that the two games mentioned are violent ones -- other ideas????
Reply | Report Abuse | Link to thisHa, this article is 3 years old but I just found it a few minutes ago.
Reply | Report Abuse | Link to thisMy space/depth perception has been predominantly monocular. I've had a touch of amblyopia from bad hyperopic anisometropia. I presume in the weaker eye the refractively corrected image from eyeglasses never focused sufficiently on the retina in the foveal region that would stimulate stereopsis. How do I know?
This past year I bought a pair of prism glasses from a stereo 3d store which enabled me to "see" the 3rd image in 2 dimensional stereograms. I was also able to use the adjuster on an Stereo Realist viewer (like a ViewMaster) to see the 3rd image in a fixed stereo pair photo. I could never see these things before. But somehow I have always been able to see 3d from colored eyeglasses and linearly polarized eyeglasses at the movies and comic books. So maybe my mis-focus hasn't been "too far" off.
Another interesting remedy for "deeper" space/depth perception has, for me, been obliquely linear polarized glasses. I use them like sunglasses. These create a "polarization disparity" which, I believe, somehow relieves the suppression instinct. Trees, leaves, branches, objects suddenly seemed out there in 3d space. Light and shade is a monocular cue supposedly, but for me the world now seems less flat in front of my eyes. The glasses also caused more dreaming at night, which I suppose is a sign of increased synaptic activity, probably improving the neural pathways. Before these glasses, I sometimes felt my brain groping for stimulation from the weaker eye so much that I even tried a flashing bike light at night under the blankets. It never worked.
I am skeptical about drug claims, like Prozac. I'm more of a natural remedy person when possible, believing that brain development has to be predominantly intelligence/perceptual based instead of predominantly chemical based.
I have yet to experiment with circular polarized stimuli.