July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Role of melanopsin in retinal light damage
Author Affiliations & Notes
  • Teele Palumaa
    Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom
  • Russell Foster
    Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom
  • Aarti Jagannath
    Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom
  • Footnotes
    Commercial Relationships   Teele Palumaa, None; Russell Foster, None; Aarti Jagannath, None
  • Footnotes
    Support  Wellcome Trust grant 090684/Z/09/Z
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 5041. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Teele Palumaa, Russell Foster, Aarti Jagannath; Role of melanopsin in retinal light damage. Invest. Ophthalmol. Vis. Sci. 2018;59(9):5041.

      Download citation file:

      © ARVO (1962-2015); The Authors (2016-present)

  • Supplements

Purpose : Melanopsin is the photopigment of photosensitive retinal ganglion cells, which mediate non-image forming responses to light, e.g. circadian entrainment and sleep, but are also important in modulating visual function via retinal circadian rhythms, dopamine metabolism and refractive development. Here we investigated the role of melanopsin in visual function and retinal photosensitivity following exposure to a bright light pulse.

Methods : Wild-type (WT) and melanopsin-deficient (Opn4-/-) mice (n=6 per group) were exposed to white light (10,000 lux) for 3 hours at zeitgeber time 16. Maximum pupil constriction, optokinetic head tracking response and visuospatial object recognition performance were measured at baseline and over 10 days after light exposure.

Results : At baseline, maximum pupil constriction was significantly attenuated in Opn4-/- mice, as reported previously (pupil area as % of maximum ± SEM, WT 5.43 ± 0.39%, Opn4-/- 9.12 ± 0.99%, p=0.006). There was no significant difference in maximum constriction in WT animals at 2, 4, 6, 8, nor 10 days after light damage compared to baseline. Interestingly, Opn4-/- mice developed an additional pupil constriction deficit by day 4 (maximum constriction 17.68 ± 2.85%, p=0.0005), which returned to baseline by day 6.
Before bright light exposure, the number of head-tracking episodes at spatial frequencies of 0.03, 0.1 and 0.4 cycles per degree (cpd) were not different between WT and Opn4-/- animals. At days 3 and 5, Opn4-/- animals followed the 0.1 cpd gratings much less compared to baseline (head tracking episodes per minute ± SEM, baseline 5.33 ± 1.09 vs 1.58 ± 0.27 at day 3, p=0.008 and 1.83 ± 0.42 at day 5, p=0.015). By day 7, this value showed a trend of recovery (3.17 ± 1.97, p=0.16).
At baseline, both WT and Opn4-/- mice spent more time of the test phase exploring the object in novel visual context than would be expected by chance (% of time spent in the novel context, WT 65%, p=0.035, Opn4-/- 66%, p=0.052). There was no difference in performance 9 days after bright light exposure.

Conclusions : We show that maximum pupil constriction and optokinetic head tracking response are impaired in Opn4-/-, but not WT mice after exposure to bright light. This deficit seems to be transient, being present only at 3-5 days after light insult. These findings suggest that the presence of melanopsin is essential in retaining normal visual function and retinal light sensitivity following light damage.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.


This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.