Most, the time spent on the screens – on computers, phones, iPads – involves many hours and often disrupts sleep. Now, the researchers of the Salk Foundation have indicated how some cells in the eye are ambient light and restore our inner clocks, the daily circles of physiological processes called circadian rhythm. When these cells are exposed to artificial light late to night, our internal clocks can be confused, resulting in a number of health issues.
The results, published November 27, 2018, at Cell Reports, it can help lead to new treatments for pigs, insomnia, weak jet and rhythm magic disorders, which are linked to cognitive discipline, cancer, obesity, insulin resistance, metabolic syndrome and more.
"We are still exposed to artificial light, be it time of a screen, spend the indoor day or staying awake late at night," said Professor Satan Panda, senior study author. "This lifestyle causes impairments to circadian rhythms and has adverse health consequences."
The eyebrows contain a sensory membrane of the retina name, whose common layer contains a small sub-gap of lightly sensitive cells that act as a pixel in a digital camera. When these cells are exposed to continuous light, a protein of the melanopsin name is continually regenerating them, indicating ambient light levels directly to the brain to regulate awareness, sleep and warning. Melanopsin plays a key role in synchronizing our internal clock after 10 minutes of lighting and, under light light, prevents the melatonin hormone, which is responsible for regulating sleeping.
"Oh compared to other cells that trigger light in the eye, melanopsin cells respond as long as the light is for, or even a few seconds longer," said Ludovic Mure , staff scientist and first author of the paper. "That's critically, because our magic clocks have been designed to respond only to long lights."
At the new work, Salk researchers used molecular tools to turn on to produce melanopsin in retina cells in mice. They find that some of these cells have the ability to hold light responses when they are exposed to long light times repeatedly, while others become insensitive.
Conventional wisdom has maintained that proteins of the name arrestinets, which prevent the activity of some receptors, prevent cell photoensitive reaction within seconds of lights. The researchers were surprised to find that arrests are actually necessary for melanopsin to continue to respond to long lights.
In mice they do not have either a version of the protein arrestin (beta arrestin 1 and beta arrestin 2), retin cells that produce melanopsin failed to maintain their light sensitivity under long lights. The reason, it's evicted, is that arrestin helps melanopsin to regenerate the retina cells.
"Our study suggests that both arrests achieve a melanopsin regeneration in a special way," said Panda. "A arrestin is his conventional arrest and reaction work, and the other helps the melanopsin protein to reload its retin-sensing light co-factor. When these two stages are quickly done, the cell appears to respond continuously to light. "
By better understanding melanopsin interactions in the body better and how the eyes respond to light, Panda hopes to discover new targets to prevent obstructive magic rhythms because, for example, artificial lighting. Previously, the Panda research team found that opsinamides called chemicals could block melanopsin activity in mice without affecting their vision, offering a potential therapeutic network to tackle hypersensitivity to light; suffering from migraine. Next, researchers aim to find ways of influencing melanopsin to reinstall internal clocks and inherent support.
This work was supported by Leona M. and the Harry B. Helmsley Charitable Trust, National Health Institutions and the Glenn Foundation.