The pupillary light reflex (PLR) controls the light intensity that reaches the retina by linking the irradiance level to the pupil diameter.
28–31 For a long time, it was thought that the PLR, and human vision in general, rely uniquely on the activation of rod photoreceptors in dim light, and short (S)-, medium (M)-, and long (L)-wavelength–sensitive cone photoreceptors in daylight, and that the information is passed on to ganglion cells via bipolar, horizontal, and amacrine cell processing.
31 However, approximately a decade ago, Lucas and colleagues
32 demonstrated that rodless and coneless rodent retinae display a reduced but measurable PLR and normal diurnal activity, which was driven by a thitherto unknown light-sensitive photopigment. Such an alternative pathway had already been suggested earlier.
33,34 Shortly thereafter, it was shown that this parallel, nonrod, noncone photoreceptive pathway arises from a separate population of photoreceptive retinal ganglion cells
35 containing the putative photopigment melanopsin.
36 By signaling gross changes in light intensity, these cells serve the subconscious, “nonimage-forming” functions of circadian photo entrainment and pupil constriction.
37–39 Since its initial discovery, several studies
40–44 have now provided evidence that melanopsin is indeed the photopigment responsible for the photo response of intrinsically photosensitive retinal ganglion cells (ipRGCs) in mice. Because the absorption maximum of melanopsin in rodents has been defined as being around 479 nm and the spectral sensitivity of these ganglion cells differs from that of rods and cones, it seemed to be possible to separate rod, cone, and melanopsin components to the PLR by their spectral sensitivity and reaction kinetics.
32