In what they believe is a solution to a 30-year biological mystery, neuroscientists say they have used genetically engineered mice to address how one mutation in the gene for the light-sensing protein rhodopsin results in congenital stationary night blindness.
In what they believe is a solution to a 30-year biological mystery, neuroscientists at Johns Hopkins Medicine say they have used genetically engineered mice to address how one mutation in the gene for the light-sensing protein rhodopsin results in congenital stationary night blindness.
When comparing the low expression level of G90D found in genetically engineered mice versus the level of G90D found in human patients with this night blindness, the authors concluded that the unusual electrical activity with a low amplitude but extremely high frequency may be the greatest contributor to the disease in people.
For decades, although researchers knew about the G90D mutation, they had difficulty determining how it caused night blindness because prior mouse models with this mutation would generate a high level of background noise, producing effects similar to background light, which the mouse's rods quickly adapt to. That made it difficult for researchers to accurately measure the mutation's signaling effects.
The scientists used a high-resolution method to record the electrical activity in individual rods in the mouse retina, which they accessed with an ultra-tiny glass pipette -- the width of about one-seventieth the size of a human hair -- filled with saline solution capable of conducting electricity. "The mechanism that causes G90D night blindness could be similar in the three other rhodopsin mutations that cause this condition," Chai says.
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