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Adaptation of Human Pineal Melatonin Suppression by Recent Photic History

Division of Sleep Medicine, Department of Medicine, Brigham & Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Charles A. Czeisler, Ph.D., M.D., Division of Sleep Medicine, Brigham & Women’s Hospital, Harvard Medical School, 221 Longwood Suite 438, Boston, Massachusetts 02115. E-mail: caczeisler{at}hms.harvard.edu.

The human circadian pacemaker controls the timing of the release of the pineal hormone melatonin, which promotes sleep, decreases body temperature, and diminishes cognitive performance. Abnormal melatonin secretion has been observed in psychiatric and circadian disorders. Although melatonin secretion is directly suppressed by exposure to light in a nonlinear intensity-dependent fashion, little research has focused on the effect of prior photic history on this response. We examined eight subjects in controlled laboratory conditions using a within-subjects design. Baseline melatonin secretion was monitored under constant routine conditions and compared with two additional constant routines with a fixed light stimulus for 6.5 h of 200 lux (50 µW/cm²) after approximately 3 d of photic exposure during the subjective day of either about 200 lux (50 µW/cm²) or about 0.5 lux (0.15 µW/cm²). We found a significant increase in melatonin suppression during the stimulus after a prior photic history of approximately 0.5 lux compared with approximately 200 lux, revealing that humans exhibit adaptation of circadian photoreception. Such adaptation indicates that translation of a photic stimulus into drive on the human circadian pacemaker involves more complex temporal dynamics than previously recognized. Further elucidation of these properties could prove useful in potentiating light therapies for circadian and affective disorders.

This work was supported in part by National Institutes of Mental Health Grant 5R01-MH45130 and National Aeronautics and Space Administration Cooperative Agreement NCC9-58 with the National Space and Biomedical Research Institute and was carried out in a General Clinical Research Center supported by National Institutes of Health Grant MO1-RR02635. K.S. also received support from the Harvard-Massachusetts Institute of Technology Division of Health Sciences and Technology. K.S. and M.S. are funded in part as research fellows on National Institutes of Health General Clinical Research Center Grant MO1-RR02635.

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