Abstract
Retinal photoreceptors modulate the pupil diameter to regulate retinal illumination. At early stage the pupilresponse 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, 1 s>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 significantly 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.