While it is difficult to do near work like reading, writing or certain crafts like needlepoint, in low light, for the most part our eyes adjust and we can maneuver in the space or at least find the light switch. How does our eyes and brain work so that we can see both in low and regular light? Also is there a way to “fix” our eyes so that those who have inherited blindness can recover some form of vision? As you can guess scientists have studied these two things and here is what they found.
Adapting to the Dark
How do our eyes make the adjustment to low light and back to regular light? The retina is able to function at varying levels of light and this is possible because of the cone and rod photoreceptors. The cone photoreceptors work best in bright light, while the rod photoreceptors work best in dim light. What keeps the rod photoreceptors from becoming over-stimulated in bright light is the movement of a subunit of the G-protein transducing from the photoreceptor’s outer segment to the inner segment.
Scientist at the National Eye Institute (NEI), studied mice who didn’t have the Frmpd1 protein, which is found in the rod photoreceptors. In this study, researchers found another protein, known as Gpsm2, which interacts with both the transducin subunit and Frmpd1. The Gpsm2 most likely helps to move the transducing subunit from the outer segments to the inner ones of the rod photoreceptor and back again. Without the Frmpd1 protein, the mouse rod photoreceptors adapted to bright light but do not adjust properly for darkness.
The results from this study suggest that there is active movement of transducing that speeds up the mouse rod photoreceptor’s ability to adapt in changing light. Knowing what goes on in the cellular level can provide insights into the movement of visual signals in the photoreceptors. Scientist want to see if there are changes in the process during early stages of inherited retinal diseases, such as retinitis pigmentosa or Leber congenital amaurosis.
Speaking of inherited retinal diseases, is it possible for adults who have Leber congenital amaurosis to see again? That is a real concern since the conventional wisdom is that circuits in the brain’s visual region must be exposed to visual stimuli during childhood in order to work properly. Once again, research shows that the conventional wisdom isn’t all that it is cracked up to be.
Scientists at the University of California, Irvine (UCI) were studying a treatment for Leber congenital amaurosis. This treatment involves the administering chemical compounds that target the retina. These compounds are called synthetic retinoids and they help to restore a good amount of vision in children with Leber congenital amaurosis. Researchers wanted to see if this treatment could help adults with this disease.
They studied adult mice that had Leber congenital amaurosis and when they administered the synthetic retinoids to the mice, the signaling in the central visual pathway was restored, especially in the circuits that process information coming from both eyes. If that wasn’t enough, the signals coming from the opposite-side eye set off two times more neurons in the brain and signals from the same side eye pathway set off five times more neurons. These results show that the visual pathways are able to be triggered and provide visual information, even after years of not being utilized.
Our eyes and brain adapt to changing conditions and research is shedding light on the how and why of these adaptations.