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

Schilling, T; Soltanlou, M; Seshadri, Y; Nuerk, H-C; Bahmani, H

doi:10.5220/0008972404820489

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Conference Paper

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

MPS-Authors

/persons/resource/persons83790

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;

External Resource

https://www.scitepress.org/PublicationsDetail.aspx?ID=LyCt5+HDgCU=&t=1
(Publisher version)

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

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: https://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.