UW Eye Research Institute -- Point of View, Fall 2006, Page 1

The important thing is not to stop
questioning. Curiosity has its own reason for existing -Albert Einstein

through scientific training and the development of an independent research program.

“I spent three years in a physiology laboratory as an undergraduate, learning about how one small change in a gene could alter the entire phenotype of an organism — the outward, observable structure. I worked on introducing a gene that caused obesity in a rat, which caused it to gain weight while eating a normal amount of food.”

Intrigued by these genetic studies, Ikeda stayed in the same laboratory to complete a PhD in Veterinary Physiology, then pursued post-doctoral studies at the Jackson Laboratory in Maine. There he studied another type of obese rodent, the “tubby” mouse, which developed retinal degeneration in addition to gaining weight. Because of this surprising finding, he became curious about the connections between nerve cells, called synapses. “My postdoctoral training introduced me to the retina of the eye, which is nerve tissue that can be viewed easily. The retina is a well-organized structure — we can see all of the layers beautifully and look directly at the differentiation of cells and cellular interactions. It makes a great research model.”

Ikeda’s UW laboratory has set a goal of understanding the synapses between nerve cells in the retina, which he believes will reveal the mechanisms underlying human diseases contributing to blindness.

In particular, Ikeda works with a mouse model of retinoschisis. Retinoschisis causes splitting of the retina into two layers, resulting in progressive loss of central and peripheral (side) vision. There are two forms of the disease in humans. The juvenile form is an inherited (genetic) condition that affects primarily boys and young men. Although the condition begins at birth, symptoms do not typically become apparent until the first years of grade school. There is also an age-related form of retinoschisis, and this type can affect both men and women and is not a genetic condition.

This cross-section of retinal layers in a two-week old mouse with retinoschisis looks relatively normal, but as the mouse ages, the layers show the characteristic splitting.

“The mouse with retinoschisis was developed by the Tennessee Mouse Genome Consortium, a center that develops mouse models of human genetic diseases. It is a perfect model for our studies. Is the retina still splitting? We can look into the eye to directly see the effects that modifying a gene has on retinal structure. Does the retina work better? We can perform the same electrophysiological tests that human patients undergo to learn about the neuronal activity following the genetic mutations we create.”

But good questions leading to promising findings are not enough. Young investigators in the first stage of their careers — like Ikeda — must compete for grant funding. During this critical time, supplemental funds are required to support lab personnel and allow for the initiation of pilot studies. One of the goals of the Eye Research Institute is to support new faculty as they establish their laboratories, and as an Institute member, Ikeda ...(Next) (Previous)