Scientists have uncovered how artificial light from smartphones and computers can disrupt sleep, a finding which may lead to new treatments for migraines, insomnia, jet lag and circadian rhythm disorders.
Researchers at Salk Institute in the US found that certain cells in the eye process ambient light and reset our internal clocks, the daily cycles of physiological processes known as the circadian rhythm.
When these cells are exposed to artificial light late into the night, our internal clocks can get confused, resulting in a host of health issues.
"This lifestyle causes disruptions to our circadian rhythms and has deleterious consequences on health," Panda said.
The backs of our eyes contain a sensory membrane called the retina, whose innermost layer contains a tiny subpopulation of light-sensitive cells that operate like pixels in a digital camera.
When these cells are exposed to ongoing light, a protein called melanopsin continually regenerates within them, signalling levels of ambient light directly to the brain to regulate consciousness, sleep and alertness.
Melanopsin plays a pivotal role in synchronising our internal clock after 10 minutes of illumination and, under bright light, suppresses the hormone melatonin, responsible for regulating sleep.
"That's critical, because our circadian clocks are designed to respond only to prolonged illumination," Mure said.
The researchers used molecular tools to turn on production of melanopsin in retinal cells in mice.
They discovered that some of these cells have the ability to sustain light responses when exposed to repeated long pulses of light, while others become desensitised.
Conventional wisdom has held that proteins called arrestins, which stop the activity of certain receptors, should halt cells' photosensitive response within seconds of lights coming on.
The researchers were surprised to find that arrestins are in fact necessary for melanopsin to continue responding to prolonged illumination.
In mice lacking either version of the arrestin protein (beta arrestin 1 and beta arrestin 2), the melanopsin-producing retinal cells failed to sustain their sensitivity to light under prolonged illumination.
The reason, it turns out, is that arrestin helps melanopsin regenerate in the retinal cells.
"Our study suggests the two arrestins accomplish regeneration of melanopsin in a peculiar way," Panda said.
"One arrestin does its conventional job of arresting the response, and the other helps the melanopsin protein reload its retinal light-sensing co-factor.
"When these two steps are done in quick succession, the cell appears to respond continuously to light," he said.
(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)