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Researchers have identified how certain cells in the eye process ambient light and reset our internal clocks, the daily cycles of physiological processes known as circadian rhythms. When these cells are exposed to artificial light late at night, our internal clocks can be disrupted, resulting in many health problems.
The study, conducted by researchers from the Salk Institute, was published in the journal Cell Reports.
The results could contribute to the development of new treatments for migraines, insomnia, jet lag and circadian rhythm disorders related to cognitive dysfunction, cancer, obesity and insulin resistance. metabolic syndrome, etc.
"We are continually exposed to artificial light, whether it's time spent in front of the screen, spending the day indoors or staying awake late at night," said Professor Salk, Satchin Panda , lead author of the study. "This lifestyle disrupts our circadian rhythms and has deleterious health consequences."
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The back of our eyes contains a sensory membrane called the retina, whose innermost layer contains a tiny population of light-sensitive cells that function like pixels in a digital camera. When these cells are exposed to continuous light, a protein called melanopsin continually regenerates within them, signaling ambient light levels directly to the brain to regulate consciousness, sleep, and alertness. Melanopsin plays a vital role in synchronizing our internal clock after 10 minutes of illumination and removes, under bright light, the hormone melatonin, responsible for regulating sleep.
"Compared to other photocells in the eye, melanopsin cells react as long as the light lasts, even a few more seconds," said Ludovic Mure, first author of the article. "It's essential because our circadian clocks are designed to respond only to prolonged illumination."
In the new work, Salk researchers used molecular tools to activate melanopsin production in retinal cells in mice. They discovered that some of these cells were able to maintain bright responses when they were exposed to repeated long pulses of light, while others became insensitive.
Conventional wisdom has argued that proteins called arrestins, which stop the activity of certain receptors, should stop the photosensitive response of cells a few seconds after illumination. The researchers were surprised to find that the arrestins are in fact necessary for melanopsin to continue to react to prolonged illumination.
In mice lacking one or the other version of the arrestin protein (beta-arrestin 1 and beta-arrestin 2), retinal melanopsin-producing cells failed to maintain their sensitivity in the light under prolonged lighting. It turns out that the reason is that the stopin helps melanopsin to regenerate in the retinal cells.
"Our study suggests that both arrestines perform the regeneration of melanopsin in a particular way," Panda said. "One artery does its conventional job of stopping the response, and the other helps the melanopsin protein to reload its co-factor for retinal light detection." When these two steps are performed in rapid succession, the cell appears to react in permanence in the light. "
By better understanding the interactions of melanopsin in the body and how the eyes respond to light, Panda hopes to find new targets to counter asymmetric circadian rhythms due to, for example, artificial illumination. Previously, the Panda research team had discovered that chemicals called opsinamides could block the activity of melanopsin in mice without affecting their vision, thus providing a potential therapeutic track to fight against. hypersensitivity to light experienced by migraine sufferers.
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