title: Dim light adaptation attenuates acute melatonin suppression in humans.
abstract: Abstract Studies in rodents with retinal degeneration indicated that neither the rod nor the cone photoreceptors obligatorily participate in circadian responses to light, including melatonin suppression and photoperiodic response. Yet there is a residual phase-shifting response in melanopsin knockout mice, which suggests an alternate or redundant means for light input to the SCN of the hypothalamus. The findings of Aggelopoulos and Meissl suggest a complex, dynamic interrelationship between the classic visual photoreceptors and SCN cell sensitivity to light stimuli, relative to various adaptive lighting conditions. These studies raised the possibility that the phototransductive physiology of the retinohypothalamic tract in humans might be modulated by the visual rod and cone photoreceptors. The aim of the following two-part study was to test the hypothesis that dim light adaptation will dampen the subsequent suppression of melatonin by monochromatic light in healthy human subjects. Each experiment included 5 female and 3 male human subjects between the ages of 18 and 30 years, with normal color vision. Dim white light and darkness adaptation exposures occurred between midnight and 0200 h, and a full-field 460-nm light exposure subsequently occurred between 0200 and 0330-h for each adaptation condition, at 2 different intensities. Plasma samples were drawn following the 2-h adaptation, as well as after the 460-nm monochromatic light exposure, and melatonin was measured by radioimmunoassay. Comparison of melatonin suppression responses to monochromatic light in both studies revealed a loss of significant suppression after dim white light adaptation compared with dark adaptation (p < 0.04 and p < 0.01). These findings indicate that the activity of the novel circadian photoreceptive system in humans is subject to subthreshold modulation of its sensitivity to subsequent monochromatic light exposure, varying with the conditions of light adaptation prior to exposure.
authors.affiliation: Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA. samar.jasser@jefferson.edu
authors.forename: Samar A
authors.initials: SA
authors.lastname: Jasser
authors.forename: John P
authors.initials: JP
authors.lastname: Hanifin
authors.forename: Mark D
authors.initials: MD
authors.lastname: Rollag
authors.forename: George C
authors.initials: GC
authors.lastname: Brainard
mesh_terms: D000221:Adaptation, Ocular; D000293:Adolescent; D000328:Adult; D002940:Circadian Rhythm; D003623:Dark Adaptation; D005260:Female; D006801:Humans; D008027:Light; D008297:Male; D008550:Melatonin / Q000378:metabolism*; D015233:Models, Statistical; D010870:Pineal Gland / Q000378:metabolism; D011863:Radioimmunoassay; D013493:Suprachiasmatic Nucleus / Q000378:metabolism; D013997:Time Factors
chemical_list: D008550:Melatonin