First some questions. Why does the retina only have one "fovea"? Why might such a region have evolved? What's the purpose of amacrine cells? Why is a ganglion cell not a good photocell just because it has a large recpetive field?

So, the structure of the eye and retinal processing demonstrate how and why what we see is largely determined by the "filling-in" of the brain. We can do little experiments to show that the brain does fill in and we know that it fills in because of the blindspot created by the optic nerve. We know the what and the why but not the how. To a certain extent, we know that lateral inhibition is the enables us to see changes in light intensity. Given this, it would make sense that we fill in with the surroundings because at the blindspot there are no photoreceptors that would allow us to detect such a change. So by deductive reasoning, if there is no change then it is the same. But why don't we just see black at every blind spot since there is no light received by the retina in this spot? Is it that the blindspot is so small in proportion to the object in vision? Is it that our brain fills in the spot after processing the state of the surroundings? Or is it more of a stretching or a bridging of the surroundings that is more the responsibility of our eye than our brain? That our brain can fill in aspects of visual stimuli suggests that it does the same for other stimuli. We know this occurs in language in which you may not "hear" every syllable of a sentence but you can fill in the missing ones using the ones you did hear. You may even report having heard every syllable and can play back the way it sounded in your head. What I don't understand is why such effects don't always occur. Is it dependent upon the quality of surrounding info you get or on previous exposure to the syllable that you missed? Probably both. Concentration obviously is also a factor.

Lots of questions (as appropriate). Isn't the large field that makes a ganglion cell not so good as a photocell but rather the fact that some areas of the field excite it, others inhibit it. Some animals have more than one "fovea" (or at least more than one area with sharper vision), others don't have much of one at all. So "foveas", like many other things in biology, work for those animals that have them (presumably making it possible to see some things more clearly). Amacrine cells mediate lateral inhibition between the middle nuclear layer and the ganglion cells and tend to be involved in motion sensitivity (which we haven't talked about but is described in at least one of the Scientific American articles).

Filling in? Yes, happens all the time. Even more than you might think. Which suggests that the "picture in the head" is actually there prior to any inputs. Then things aren't so much filled in as left undisturbed. Its actually an active area of research, so if you're particularly interested I'd be happy to give you some places where you could read about it. PG