Nature 453, 102-105 (1 May 2008) | doi:10.1038/nature06829; Received 11 July 2007; Accepted 7 February 2008; Published online 23 April 2008

Melanopsin cells are the principal conduits for rod–cone input to non-image-forming vision

Ali D. Güler1,7, Jennifer L. Ecker1,7, Gurprit S. Lall2,7, Shafiqul Haq3, Cara M. Altimus1, Hsi-Wen Liao3, Alun R. Barnard2, Hugh Cahill3, Tudor C. Badea4, Haiqing Zhao1, Mark W. Hankins5, David M. Berson6, Robert J. Lucas2, King-Wai Yau3 & Samer Hattar1

  1. Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218, USA
  2. Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, UK
  3. Department of Neuroscience, and,
  4. Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
  5. Visual Neuroscience, University of Oxford, Oxford OX3 7BN, UK
  6. Department of Neuroscience, Brown University, Providence, Rhode Island 02912, USA
  7. These authors contributed equally to this work.

Correspondence to: Robert J. Lucas2Samer Hattar1 Correspondence and requests for materials should be addressed to S. Hattar (Email: shattar@jhu.edu) or R.J.L. (Email: robert.lucas@manchester.ac.uk).

Rod and cone photoreceptors detect light and relay this information through a multisynaptic pathway to the brain by means of retinal ganglion cells (RGCs)1. These retinal outputs support not only pattern vision but also non-image-forming (NIF) functions, which include circadian photoentrainment and pupillary light reflex (PLR). In mammals, NIF functions are mediated by rods, cones and the melanopsin-containing intrinsically photosensitive retinal ganglion cells (ipRGCs)2, 3. Rod–cone photoreceptors and ipRGCs are complementary in signalling light intensity for NIF functions4, 5, 6, 7, 8, 9, 10, 11, 12. The ipRGCs, in addition to being directly photosensitive, also receive synaptic input from rod–cone networks13, 14. To determine how the ipRGCs relay rod–cone light information for both image-forming and non-image-forming functions, we genetically ablated ipRGCs in mice. Here we show that animals lacking ipRGCs retain pattern vision but have deficits in both PLR and circadian photoentrainment that are more extensive than those observed in melanopsin knockouts8, 10, 11. The defects in PLR and photoentrainment resemble those observed in animals that lack phototransduction in all three photoreceptor classes6. These results indicate that light signals for irradiance detection are dissociated from pattern vision at the retinal ganglion cell level, and animals that cannot detect light for NIF functions are still capable of image formation.


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