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Blue Light and Melanopsin Contribution to the Pupil Constriction in the Blind-spot, Parafovea and Periphery

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Bahmani,  H
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;
Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Citation

Schilling, T., Soltanlou, M., Seshadri, Y., Nuerk, H.-C., & Bahmani, H. (2020). Blue Light and Melanopsin Contribution to the Pupil Constriction in the Blind-spot, Parafovea and Periphery. In F. Cabitza, A. Fred, & H. Gamboa (Eds.), BIOSTEC 2020: Proceedings of the 13th International Joint Conference on Biomedical Engineering Systems and Technologies (pp. 482-489). Setúbal, Portugal: Scitepress.


Cite as: http://hdl.handle.net/21.11116/0000-0006-FF4C-7
Abstract
Retinal photoreceptors modulate the pupil diameter to regulate retinal illumination. At early stage the pupil-response is formed by intrinsically-photosensitive-Retinal-Ganglion-Cells (ipRGCs) expressing melanopsin, activated by blue light. ipRGCs’ axons pass through the optic nerve head, corresponding to the blind-spot. No photoreceptors except melanopsin appear to exist in the blind-spot. Contributions of melanopsin to pupil constriction in absence of classical photoreceptors in the blind-spot is not fully understood. We investigated how blue light in the blind-spot changes melanopsin-pupil-response compared to parafovea and periphery. The Post-Illumination-Pupil-Response (PIPR) amplitude reflecting melanopsin was analyzed for standardized time windows (1s<1.7s, 1s>1.8s and 2–6s) and expressed as pupillary-change. Bayesian analysis showed a BF>3 that PIPR>1.8s for blind-spot and periphery is not different. At times 2s–6s, a t-test comparison in the blind-spot condition showed a sign ificantly larger PIPR to blue compared to red light, confirming a melanopsin-pupil-response in the blind-spot. Taken together, equivalent stimulation in the blind-spot and periphery revealed comparable PIPR, although there are no rods and cones in the blind-spot. In absence of classical photoreceptors in the blind-spot, melanopsin seems to be responsible for pupil constriction in similar manner as in the periphery, which supports the presence of melanopsin on the axons of ipRGCs.