A key role in synchronizing daily rhythms to the day/night cycle has been traced to a light-sensitive protein in the eye, by knocking out the gene that codes for it. Mice lacking a gene for the photopigment melanopsin show a dramatic deficiency in their ability to regulate their circadian rhythms by light. The discovery, by National Institute of Mental Health (NIMH) grantees, helps unravel the heretofore elusive mechanisms by which day/night cycles regulate such rhythms in mammals. NIMH grantees Ignacio Provencio, Ph.D., Uniformed Services University of the Health Sciences (USUHS), and Steve Kay, Ph.D., The Scripps Research Institute, and colleagues report on their findings in the December 13 Science.*
In a similar knockout mouse study reported in the same issue of Science, another research team, led by NIMH grantee Norman Ruby, Ph.D., Stanford University, also found melanopsin to be a "significant contributor" to circadian function.**
Each day, a clock in the brains hypothalamus that governs daily rhythms – sleeping/waking, body temperature, eating, arousal. -- is reset by light detected in the eyes. Yet, how this works has been a mystery. Light can still reset the clock even if the rods and cones, the photoreceptors in the retina for vision, are removed, but not if the eyes are removed. Hence, scientists have hypothesized that the eyes must contain a system of photoreceptors for resetting the clock that is separate from the system for sight.
Jules Asher | EurekAlert!
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