Ichneumonwasp
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- Feb 2, 2006
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Here:
http://www.jneurosci.org/cgi/reprint/20/24/9310.pdf
(FYI I should keep my amateur research more organized... I can hardly find the papers I actually read to come to conclusions... I just grabbed this one from a google search of "V1 blind spot").
Essentially in V1 all of our perceptual field is mapped, including the area of our blind spot, surprisingly enough. For some reason. But it's there.
I spent part of the morning racking my brain about the ways that we 'overcome' the blind spot, and I seem to recall three different mechanisms -- two in the eye itself and one in the occipital cortex. I'm not sure how much each of these matters, but I think they probably all play a role. Only one of them leads to what I would call "filling in", but as you know I don't like that way of expressing things with this issue.
I really should have just looked this up since I haven't though about the issue for more than 20 years, but this is what I can come up with trying to dredge up old memories.
First, we don't form visual images except on a somewhat slow time scale compared to the micro level. During the time in which we form a new image the eye moves, since our eyes are constantly moving -- in fact, without saccades we probably couldn't see anything.
Second, there is some level of filling in, as I recall, at the level of the ganglion cells, though this might be amplified at later levels. The visual fields of ganglion cells, if memory serves, is a bit fuzzy and enlarged compared to the receptors themselves -- to the extent that a first attempt is made to accentuate contrast to limit these fields. I can't recall the names of the cells that provide negative input to the ganglion cell layer to produce the first instantiation of center-surround inhibition, but that process is already going on in the retina. The cells immediately adjacent to the optic nerve don't have receptors next to them (where the optic nerve is), so they only have surround inhibition on one side -- leaving them, if memory serves, with a larger center that "bleeds into" the area of the blind spot. This is a relatively minor issue, though, and I don't think the fields are big enough to cover the entire blind spot.
Third, the blind spots of both eyes are in different visual hemifields, so that the visual information from one eye can supply what is missing from the other. When there is an imbalance in visual input from early in development one of inputs is suppressed -- the same thing happens in kids with a tropia or strabismus since the visual information from one eye is suppressed and that eye goes blind (amblyopia). Visual info from both eyes ends up in the same place so that we see visual hemifields (not to be confused with the visual fields of individual cells), allowing for binocular vision. Any lack of info from the 'blind spot' would simply be suppressed by the visual cortex.
There may be more mechanisms having to do with the visual fields of cells in the cortex and the ways they are constructed, but that's all could think of this morning.