Discovery explains how cells in the eye sense light and adjust our circadian rhythms
A remarkable study from researchers at the Salk Institute hasuncovered a profound new insight into how our circadian rhythms areregulated through light-sensing mechanisms within our eyes. Theresearch could lead to new ways to combat insomnia and help reset theinternal clocks of people with disrupted circadian rhythms.
We know that our circadian rhythms are fundamentally driven byexposure to light, and we also know that artificial blue light candisrupt those natural 24-hour rhythms. But how do our bodies activelysense light and adapt their circadian rhythm accordingly? Well, itcomes down to a small volume of retinal cells in the back of our eyesand a recently discovered light-sensitive retinal protein calledmelanopsin.
Melanopsin was only identified less than two decades ago and its discovery helped define a new class of retinal cells. Alongside therods and cones in our eyes we have a small amount of innatelyphotosensitive cells. These cells are designed to not help us see,but rather sense light as part of our circadian management system.
When these specific retinal cells sense light, they produce melanopsin, which directly tells certain parts of ourbrain to stay awake and alert. As well as suppressing melatonin,melanopsin has been found to help regulate and set our body'scircadian rhythm.
"Compared to other light-sensing cells in the eye, melanopsincells respond as long as the light lasts, or even a few secondslonger," says Ludovic Mure, first author of the paper. "That'scritical, because our circadian clocks are designed to respond onlyto prolonged illumination."
The new study set out to uncover exactly what molecular mechanismoccurs when melanopsin cells are triggered by light. Generally,proteins called arrestins act to block the activity of certainreceptors, however, this research unexpectedly revealed that the continualmelanopsin activity in the eye was actually maintained by theinteraction between two particular arrestins.
Animal studies revealed that two arrestins (beta arrestin 1 andbeta arrestin 2) worked together to maintain continued melanopsinactivity in the presence of light stimulation. When one of thosearrestins was blocked, melanopsin regeneration was disruptedsuggesting this mechanism helps manage the continual signal to thebrain that there is light and we should stay alert.
"Our study suggests the two arrestins accomplish regeneration ofmelanopsin in a peculiar way," says Satchidananda Panda, seniorauthor on the study. "One arrestin does its conventional job ofarresting the response, and the other helps the melanopsin proteinreload its retinal light-sensing co-factor. When these two steps aredone in quick succession, the cell appears to respond continuously tolight."
The hypothesis following on from this research is that byunderstanding how light sensed by the eye can help set our circadianrhythm, we can hopefully produce treatments for a huge variety ofdisorders. If light from our digital screens is artificiallyoverstimulating melanopsin and disrupting our circadian rhythm, maybethis mechanism can be interrupted using drugs. Or maybe some peoplesuffering from insomnia could have their circadian clocks chemicallyreset by triggering this mechanism. Panda and the research team atSalk will be turning their focus towards these questions for the nextstages of their work.
The new study was published in the journal Cell Reports.
Source: Salk Institute