You and I, as well as all of our mammalian brethren, have just a few photopigments, i.e., colored molecules that change shape when exposed to light and subsequently trigger cascades of biochemical reactions leading to changes in electrical properties of sensory neurons, which lead to modulation of neurotransmitter release, which propagates the information from one neuron to the next until it is integrated and interpreted somewhere in the brain - we see the light!
More under the fold....
Mammals have rhodopsin (in rod-shaped photoreceptor cells in the retina of the eye), three or four color-opsins (in the cone-shaped photoreceptor cells in the retina) and melanopsin (in the retinal ganglion cells). Rhodopsin is a pigment of basic vision and allows us to see shapes and movement both day and night. Color-opsins are each tuned to a different wavelength of light, allowing us to see color, best during the day. Melanopsin is involved in unconscious, non-visual photoreception: control of iris diameter, entrainment of circadian rhythms and control of mood.
While the rods and cones project to the visual processing region in the occipital portion of the cerebral cortex, photosensitive ganglion cells project to other places in the brain, including centers involved in the control of mood, and the circadian pacemakers in the suprachiasmatic nucleus of the hypothalamus (at the base of the brain).
Rods and cones have evolved some particular adaptations to visual perception, including fast desensitization - you do not need to see the image of the tiger attacking you for a long time after the tiger has already moved away from that spot. These photoreceptors have to move fast in order to track the events in real time. The integration of visual information starts already in the eye - horizontal and bipolar cells in the retina work on providing greater contrast, thus making the image sharper.
On the other hand, photoreceptive retinal ganglion cells serve a different function - as lightmeters. They do not show desensitization. If it is 1000lux outside one moment and 1000lux the next moment, you do not want your lightmeter to give you different readings at those two moments (e.g., 1000lux the first moment and 10lux the next moment due to desensitization). They have evolved to work slowly.
Now, if you think this is all very complicated, think again. This is a super-simplified system compared to all other vertebrates.
Lampreys, some fish, some amphibians and some reptiles have a frontal (or parapineal) organ on the top of their heads, often with a lens and organization of the epithelium similar to that of the retina. Those organs use a completely different set of photopigments, including color-opsins. These organs may not form perfect images, but they can detect, for instance, rough outlines of shadows of predators flying overhead and track that in real time. They can also distinguish between blue (sky) and green (foliage) colors in a strange way - stimulation of the blue receptors inhibits the green receptors and vice versa.
The retina of non-mammalian vertebrates also possesses at least two more different color-opsins, allowing these animals to see, for instance, well into the ultraviolet range.
Except in mammals and snakes, the pineal organ is also directly photosensitive, utilizing, among else, a photopigment called pinopsin. In many species of non-mammalian vertebrates, from lampreys, through Diplodocus, to birds, the pineal organ is located at the surface of the brain and the skull just above it is either thinner or has a hole in it. Shining light onto the pineal immediately inhibits production of melatonin at night and, more slowly, resets the circadian clock in species in which the circadian pacemaker is located in the pineal organ (e.g., sparrows).
Some regions deep inside the brain of all non-mammalian vertebrates, e.g., the median eminence, are also directly photoreceptive and are involved in light effects on the circadian clock as well as photoperiodic control of seasonality. Light easily passes through the skin, skull and brain mass (take a flashlight and shine the light through your hand or under the chin to see how much light can penetrate living tissues!). These regions have not been well characterized molecularly, but it appears that an opsin related to invertebrate photopigments may be involved in this area.
Finally, in some fish, skin is photosensitive and a circadian clock located in each cell of the body is directly photosensitive as well. In sea-snakes, the skin on the tail is directly photosensitive and it mediates photokinesis (behavioral response to light, i.e., attack).
But it is not just at the anatomical level that the non-mammalian photoreception is much more complex than that in the mammals. Mammals have a pitiful number of molecules involved - the 5-6 photopigments I listed above. Each of those photopigments is coded by a single copy of a single gene.
I have already noted that non-mammalian vertebrates have additional photopigments, e.g., pinopsin, color-opsins in the frontal organ, invertebrate-like opsins in the deep brain receptors, and additional color opsins (including UV-opsin) in the retina. Moreover, unlike in mammals, some of those pigments are coded by two or more copies of the gene, each resulting in a slightly different light-sensitive protein.
How do various light-sensitive proteins differ from each other? They respond to slightly different wavelengths of light ("colors") and may also respond with different dynamics (e.g., slower or faster). The speed of 'recovery' or replacement will also differ. Each may also be "hooked onto" a different cascade of biochemical events downstream from the photopigment resulting in a different cellular response. You can already see how such a complex system allows for much better fine-tuning of vision and non-visual photoreception than in mammals.
For instance, the spectral composition of light changes during the course of the day. While mammals may have to rely primarily on light intensity and only crudely to spectral composition in order to figure out the time of day (especially if, as most small mammals do, they spend most of the time underground in the dark), the non-mammalian vertebrates can have a finely evolved "map" of spectral composition and be able to determine time of day with much greater precision irrespective of light intensity (cloudy day, for instance).
The story about melanopsin just got more complex today with a new paper published in PLoS-Biology, by a bunch of top circadian and photobiologists working together. You can read the excellent short synopsis or try to plow through the difficult actual paper (text) (PDF). It is a very impressive piece of work.
Apparently, there are actually two classes of melanopsin gene. One class is found in all vertebrates, including mammals. Mammals have one copy of it, while some fish have multiple copies (with some variation in sequence). But all vertebrates EXCEPT mammals (including both placentals and marsupials) also have a melanopsin from a different class.
So, it appears that the melanopsin gene got duplicated very early in vertebrate evolution and each evolved in its own direction.
One of the copies got subsequently duplicated (and then duplicated again) in fish.
One of the copies then, much later (probably in the Jurassic), got lost through deletion from the genome of early mammals.
Melanopsin is expressed in a very small number of cells in mammals - just a few thousand retinal ganglion cells in each eye. In contrast, both classes of melanopsin genes are expressed broadly in all non-mammalian vertebrates - in several layers of the retina, in the pineal, and in several other parts of the brain.
The speculative hypothesis for the "Why" question is that mammals underwent a reduction in photoreceptive capabilities during 150 million years of the Reign of Dinosaurs. During that time, all mammals were tiny, nocturnal, subterranian critters. That was the only niche they could occupy during this period unless they wanted to get eaten by T-rex on a regular basis.
They evolved exquisite senses of smell and hearing (and touch, via whiskers), and lost much of their visual acuity, as well as non-visual perception (i.e., extraretinal photoreception). The loss of visual acuity was compensated later by refining the anatomy of the eye and the organization of the brain instead of re-evolving the lost photopigments and spreading their expression to tissues outside the eye.
I hope that this paper promotes further work on functional studies of the two melanopsin classes to see how they differ from each other. This, of course, has to be done in a non-mammalian vertebrate, which is a hard sell to the NIH these days. Perhaps this paper can help in this regard. Not everything can be lerarned from mice and rats.
Thanks for a very interesting post! This is why I read ScienceBlogs - great articles explaining science clearly so an amateur with a smattering of bio courses can understand. (ok, I come for the snark, too, but the science is just way cool.)
I read the headline and thought, "I'll say! I didn't even know I had a pet iguana!"
Fascinating post. I think my photoreceptor cells blushed when they realized you were talking about them.