Influence of Light Exposure on the Melanopsin Driven Pupil Response and Circadian Rhythm
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Exposure to increasing amounts of artificial light during the night may contribute to the high prevalence of reported sleep dysfunction. Release of the sleep hormone melatonin is mediated by the intrinsically photosensitive retinal ganglion cells (ipRGCs). ipRGCs signal environmental light, with pathways to the midbrain to control pupil size and circadian rhythm. Evidence suggests that light exposure plays a role in refractive error development. This study sought to investigate whether melatonin level and sleep quality can be modulated by decreasing nighttime input to the ipRGCs. Another goal was to investigate links between light exposure, ipRGCs, refractive error, and sleep. Methods: Experiment 1: Subjects (ages 17-42, n=21) wore short wavelength-blocking glasses prior to bedtime for two weeks. The ipRGC-mediated post illumination pupil response (PIPR) was measured before and after the experimental period. Stimulation was presented with a Ganzfeld stimulator, including 1 second (s) and 5 s long and short wavelength light, and the pupil was imaged with an infrared camera. Pupil diameter was measured before, during and for 60 s following stimulation, and the 6 s and 30 s PIPR and area under the curve (AUC) following light offset were determined. Subjects wore an Actigraph device for objective measurements of activity, light exposure, and sleep. Saliva samples were collected to assess melatonin content. The Pittsburgh Sleep Quality Index (PSQI) was administered to assess subjective sleep quality. Experiment 2: Fifty subjects, aged 17-40, participated (19 emmetropes and 31 myopes). A subset of subjects (n = 24) wore an Actiwatch Spectrum for one week. The Pittsburgh Sleep Quality Index (PSQI) was administered, and saliva samples were collected for melatonin analysis. The post illumination pupil response (PIPR) to 1 second (s) and 5s long and short wavelength stimuli was measured. Pupil metrics included the 6s and 30s PIPR and early and late area under the curve. Results: Experiment 1: Subjects wore the blue-blocking glasses 3:57 ± 1:03 hours each night. After the experimental period, the pupil showed a slower redilation phase, resulting in a significantly increased 30 s PIPR to 1 s short wavelength light, and decreased AUC for 1 s and 5 s short wavelength light, when measured at the same time of day as baseline. Nighttime melatonin increased from 16.1 ± 7.5 pg/mL to 25.5 ± 10.7 pg/mL (p < 0.01). Objectively measured sleep duration increased 24 minutes, from 408.7 ± 44.9 to 431.5 ± 42.9 minutes (p < 0.001). Mean PSQI score improved from 5.6 ± 2.9 to 3.0 ± 2.2. Experiment 2: Subjects spent 104.8 ± 46.6 minutes outdoors per day over the previous week. Morning melatonin concentration (6.9 ± 3.5 pg/mL) was significantly associated with time outdoors and objectively measured light exposure (P = 0.0099 and 0.0016, respectively). Pupil metrics were not significantly associated with light exposure or refractive error. PSQI scores indicated good sleep quality for emmetropes (score 4.2 ± 2.3) and poor sleep quality for myopes (5.6 ± 2.2, P = 0.036). Conclusions: The use of short wavelength-blocking glasses at night increased subjectively measured sleep quality and objectively measured melatonin levels and sleep duration, presumably as a result of decreased nighttime stimulation of ipRGCs. Alterations in the ipRGC-driven pupil response suggest shift in circadian phase. Results suggest that minimizing short wavelength light following sunset may help in regulating sleep patterns. Additionally, morning melatonin levels were influenced by light exposure and time outdoors. No differences in melatonin or the ipRGC-driven pupil response were observed between refractive error groups, although myopes exhibited poor sleep quality compared to emmetropes. Findings suggest that a complex relationship between light exposure, ipRGCs, refractive error, and sleep exists.