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Blue Light and Melanopsin Contribution to the Pupil Constriction in the Blind-spot, Parafovea and Periphery
{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\textquoteright 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\textless1.7s, 1s\textgreater1.8s and 2\textendash6s) and expressed as pupillary-change. Bayesian analysis showed a BF\textgreater3 that PIPR\textgreater1.8s for blind-spot and periphery is not different. At times 2s\textendash6s, 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.}
@inproceedings{item_3252211, title = {{Blue Light and Melanopsin Contribution to the Pupil Constriction in the Blind-spot, Parafovea and Periphery}}, booktitle = {{BIOSTEC 2020: Proceedings of the 13th International Joint Conference on Biomedical Engineering Systems and Technologies}}, 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\textquoteright 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\textless1.7s, 1s\textgreater1.8s and 2\textendash6s) and expressed as pupillary-change. Bayesian analysis showed a BF\textgreater3 that PIPR\textgreater1.8s for blind-spot and periphery is not different. At times 2s\textendash6s, 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.}}, volume = {5}, pages = {482--489}, publisher = {Scitepress}, address = {Valletta, Malta}, year = {2020}, slug = {item_3252211}, author = {Schilling, T and Soltanlou, M and Seshadri, Y and Nuerk, H-C and Bahmani, H} }