Although doctors have known about the existence of protein α2δ4 for years, it's only now that eye doctors are getting seriously interested in exploring α2δ4's potential in eye care treatment. The renewed interest in this protein is mainly due to recent research conducted at Scripps Research Institute (TSRI) in Juniper, Florida. TSRI researchers have just released their findings that show a clear link between α2δ4 and photoreceptor communication.
Scientists used a group of mice to study the effects of α2δ4 on the eyes. All of the mice chosen in this study already had retinal dystrophy.
Professor Kirill A. Martemyanov, the head researcher on this study, said that α2δ4 immensely helps the rod photoreceptors in the eyes pick up and send light signals to the brain. This function of α2δ4 is the primary reason mice without the protein experience more pronounced symptoms of poor color vision and night blindness.
The researchers at TSRI have been running tests on the eyes for decades now in an attempt to better understand the nature of sight. In a previous study, scientists were able to identify the cell-adhesion protein ELFN1 that helps rod photoreceptors in the retina contact each other.
TSRI Research Associate Yuchen Wang was another key researcher on this study. Wang's main interest was studying how ELFN1 helps with photoreceptor communication. Throughout his research, Wang soon discovered ELFN1 accomplishes its communication tasks by binding with various proteins such as α2δ4. These connections create what are called "calcium channels," which in turn helps to release the messenger chemical glutamate.
Whenever the researchers purposefully removed α2δ4 in mice with retinal dystrophy they found that the photoreceptors in the mice's eyes weren't able to transmit light signals to the brain. Scientists placed mice without α2δ4 in dimly lit rooms and observed how well they were able to make it through a maze. Unsurprisingly, all of these mice struggled to make their way successfully through this maze due to their dysfunctional rods.
Although these rod photoreceptors couldn't function properly without α2δ4, the ability for the mice's eyes to pick up light was still functional. Martemyanov explained this phenomenon by using the analogy of a phone call. When you take the α2δ4 out of the eye, it's just like using a working phone that isn't able to pick up your voice due to a poor signal.
Looking ahead, researchers hope they will be able to develop new treatment methods with α2δ4 to stave off the symptoms of age-related eye diseases like retinal dystrophy. Martemyanov is hopeful his team's recent findings will help scientists develop novel treatments to help dying photoreceptors send stronger signals to the brain.
Most eye doctors nowadays are only interested in injecting stem cells into the eyes to combat diseases like retinal dystrophy and age-related macular degeneration. Although stem cell treatment may be beneficial, Martemyanov believes researching the effects of increased α2δ4 in human subjects should receive more attention from the medical community as a viable way to reduce the symptoms of certain potentially blinding diseases.
Martemyanov's latest study was recently published in the journal Neuron under the title "The Auxiliary Calcium Channel Subunit α2δ4 Is Required for Axonal Elaboration, Synaptic Transmission, and Wiring of Rod Photoreceptors."