Last week, we explained what light is all about. But how do we know light exists?
It’s because those of us fortunate enough to have largely unimpaired vision can “see” it. We’re equipped with a very complex visual system that can convert the energy associated with light into electrical energy. These electrical impulses then travel to our brains, carrying information from the light around us. In areas such as the visual cortex (and others), we then reassemble and perceive these complex images. The images are then tucked away into memory, or elicit another physical, emotional or mental response.
This entire series of events, however, relies on one important and complex first step: visual transduction. When light first hits the eye, it travels to a specialized region in the back called the retina. The retina houses receptors capable of converting light into the nervous system’s mode of communication (called the “action potential”). These receptors are called rods and cones. Rods are generally sensitive to all wavelengths of light and allow for nighttime “gray” vision. In contrast, cones are sensitive to specific wavelengths of light and allow for daytime color vision. Light first stimulates these two classes of photoreceptors, which then relay their information to a group of neurons called bipolar cells. Bipolar cells then transmit their signals to another class of neurons called retinal ganglion cells. Finally, these retinal ganglion cells use long projections, called axons, to take the visual information out of the retina and into higher areas of the brain.
This circuitry, when intact, allows us to see the reality that light illuminates. But if it fails, our visual perception also disappears. We can’t convert the stimulation of light into a language that our brain understands. And when this happens, blindness ensues. In diseases such as retinitis pigmentosa and age-related macular degeneration, the rods and cones of the retina degenerate, causing blindness.
This circuitry, when intact, allows us to see the reality that light illuminates.
In February 2014, researchers at the University of California, Berkeley, found a way to restore the retina’s ability to respond to light in cases where the rods and cones have deteriorated. In a paper published in Neuron, Richard Kramer and his team were able to introduce a small molecule called DNAQ into the retina. This molecule, a chemical “photoswitch,” was found to make the retina of previously blind mice sensitive to light. Specifically, when a solution of DNAQ was injected into the mouse retina, the retina was able to respond to an intensity of white light similar to that of daylight. DNAQ was also found to restore light-elicited behavior and enable visual learning in mice that had previously lost light sensitivity due to degenerated photoreceptors. No toxicity was reported in the mice — that is, they experienced no apparent adverse effects as a result of the treatment.
Kramer and his team hope that DNAQ will provide an alternative to the current methods of restoring vision in patients with degenerative retinal diseases. Since existing techniques are both invasive and irreversible, DNAQ potentially presents a non-invasive and low-risk method of making the retina sensitive to light. And with the advent of such a technique, it is possible that even fewer people will ever find themselves questioning the existence of light.
This piece is part of a series of short, biweekly(ish) columns on topics of general interest, including common-sense explanations of complex scientific phenomena. Stay tuned for more!
For a global health perspective on visual impairment, see this article.
- Restoring Visual Function to Blind Mice with a Photoswitch that Exploits Electrophysiological Remodeling of Retinal Ganglion Cells. Tochitsky, Ivan et al. Neuron, Volume 81, Issue 4, 800 – 813.
Atrin Toussi is a Brevia Primary Research Co-editor. She can be reached at firstname.lastname@example.org.