Spend enough time around eye doctors or in my case, reading about eye and vision research and you will learn that the eyes are the front of the brain. While the eyes are taking in the visuals, it is the brain that is interpreting them. Most of time, things work correctly, and people see what they need to see in order to work and maneuver through their surroundings. If something isn’t working correctly, is it possible to “fix” it, either through biological or pharmaceutical means? Two research projects, one at Columbia University and another at University of California, Irvine found that it is possible to “fix” what isn’t working.
Research at Columbia University studied the eyes of albino mice. The lab of Carol A. Mason, PhD has studied for many years how the axons of the retinal ganglion cells in a developing visual system find their way to the correct destination. Her lab found that receptors on cells to respond to molecular signals in a type of neural crossover hub. This is where the growing axons from the retinal ganglion cells split. Some progress along the same side of the retina to a visual center deep in the brain, while others cross over to the other side of the brain as they make those connections.
In this study, scientists wanted to know when and where the retinal ganglion cells get the idea to crossover or not. It was found that the depends on when the cells first formed a niche within the rim of the retina. For each cell, the time it is “born” determines if genes for a left-progressing or right-progressing path of its axon becomes active. Since the albino mouse’s right-left distribution is imbalanced, it is a good model for studying this process. The end result of this imbalance lead to a disruption of binocular vision and to impaired depth perception.
Researchers compared the cell-birthing process in both typical and albino mouse retinas. Scientists were able to see the progression of cell formation and differentiation in the developing retina by grouping cells based on gene activity. What they saw was that the cell formation in the retina of the albino mice was disturbed compared to the retinas of the typical mice. In fact, many of the albino mice’s retinal ganglion cells developed too late for gene associated with same-side axonal growth to be activated. This glitch changed to which side of the brain axons from each eye tend to connection. This led to the depth perception impairment in the albino mice.
Is this defect permanent or can it be reversed? Scientists found a gene that controls cell birthing and found that it was disrupted in albino mice. They also found that using a drug to accelerate this gene in albino mice pups helped the axons to connect to the right place and behavioral studies demonstrated that this improved the mice’s depth perception.
What about “fixing” vision after a disease has done its damage? Can that be done? Researchers in the lab of Sunil Gandhi, professor of neurobiology and behavior at University of California, Irvine (UCI) found that it can be done.
When children with Leber congenital amaurosis (LCA), which is a group of inherited retinal diseases that cause visual impairment at birth, are given synthetic retinoids they can have a good amount of vision restored. Researchers at UCI School of Biological Sciences and the School of Medicine wanted to see if the synthetic retinoids could help adults who have this condition.
They worked with rodent models of LCA and found that central visual pathway signaling was “significantly” restored in adult mice who received the synthetic retinoids. Signals coming from the opposite-side eye activated two times more neurons in the brain, immediately after receiving the treatment. In fact, the signals coming from the same-side eye pathway activated five-fold more neurons in the brain after treatment and this effect was long lasting.
Prior to this research, it was thought that the brain must receive visual signals in childhood so that the circuits would work correctly. This study supports the idea that there is latent potential for vision that is waiting to be activated.
“Whenever you have a discovery that breaks with your expectations about the possibility for the brain to adapt and rewire, it teaches you a broader concept,” Gandhi said. “This new paradigm could aid in the development of retinoid therapies to more completely rescue the central visual pathway of adults with this condition.”
These research projects show that it is possible to fix what is broken and make it better.