Photic Regulation of Melatonin in Humans: Ocular and Neural Signal Transduction

Author:

Brainard George C.1,Rollag Mark D.2,Hanifin John P.1

Affiliation:

1. Department of Neurology, Thomas Jefferson University, Jefferson Medical College, Philadelphia, PA 19107

2. Department of Anatomy, Uniformed Services University of Health Sciences, Bethesda, MD 20814

Abstract

Light is a potent stimulus for regulating the pineal gland's production of melatonin and the broader circadian system in humans. It initially was thought that only very bright photic stimuli (≥ 2500 lux) could suppress nocturnal melatonin secretion and induce other circadian responses. It is now known that markedly lower illuminances (≤ 200 lux) can acutely suppress melatonin or entrain and phase shift melatonin rhythms when exposure conditions are optimized. The elements for physical/biological stimulus processing that regulate photic influences on melatonin secretion include the physics of the light source, gaze behavior relative to the light source, and the transduction of light energy through the pupil and ocular media. Elements for sensory/neural signal processing become involved as photons are absorbed by retinal photopigments and neural signals are generated in the retinohypothalamic tract. Aspects of this physiology include the ability of the circadian system to integrate photic stimuli spatially and temporally as well as the wavelength sensitivity of the operative photoreceptors. Acute, light-induced suppression of melatonin is proving to be a powerful tool for clarifying how these elements of ocular and neural physiology influence the interaction between light and the secretion of melatonin from the human pineal gland.

Publisher

SAGE Publications

Subject

Physiology (medical),Physiology

Reference34 articles.

1. Peripheral vision suppression of melatonin

2. Barker FM and Brainard GC (1991) The Direct Spectral Transmittance of the Excised Human Lens as a Function of Age (FDA 785345 0090 RA), U.S. Food and Drug Administration, Washington, DC.

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