this page, allowed us to see the difference at a glance. Clearly something had gone wrong, with a vengeance.
We soon repeated the experiment in more kittens and in baby monkeys. In kittens, a larger series soon showed that if an eye is closed at birth, on the average only 15 percent of cells prefer the eye that was closed, instead of about 50 percent. The same results were found in monkeys (see the bottom histogram). Of the few cells that did respond through the eye that had been closed, many seemed abnormal; they fired sluggishly, fatigued easily, and lacked the normal precise orientation tuning.
A result like this raises many questions. Where in the visual path was the abnormality? In the eye? The cortex? Could the cat see with the eye that had been closed, despite the cortical abnormality? Was it light or form deprivation that produced the abnormality? Was the age at which we closed the eye important? Was the abnormality a result of disuse or of something else? To get answers to such questions took a long time, but we can state the results in a few words.
The obvious way to determine the site of the abnormality was to record at lower levels, starting, say, in the eye or the geniculate. The results were unequivocal: both the eye and the geniculate had plenty of cells whose responses were virtually normal. Cells in the geniculate layers that received input from the eye that had been closed had the usual center-surround receptive fields;
they responded well to a small spot and poorly to diffuse light. The only hint of abnormality was a slight sluggishness in the responses of these cells, compared with the responses of cells in the layers fed by the normal eye.
Given this relative normality, we were amazed when we first saw the Nisslstained lateral geniculate under the microscope. It was so abnormal that a microscope was hardly needed. The cat's geniculate has a somewhat more simple organization than the monkey's; it consists mainly of two large-cell layers, which are on top rather than on the bottom, as in the monkey. The upper layer receives input from the contralateral eye, the lower from the ipsilateral. Beneath these layers is a rather poorly defined small-cell layer with several subdivisions, which I will ignore here. On each side, the large-cell layer receiving input from the closed eye was pale and clearly thinner than its companion, which looked robust and perfectly normal. The cells in the abnormal layers were not only pale but were shriveled to about two-thirds their normal cross-sectional area. This result for a right-eye closure is shown in the photographs on the next page. Similar results were found in the macaque monkey k for a right-eye closure, as shown in the photograph below. We thus faced a paradox that took us a few years to explain: a lateral geniculate whose cells seemed relatively normal physiologically but were manifestly pathological histologically. Our original question was in any case answered, since cortical cells, although virtually unresponsive to the closed eye, were evidently receiving a substantial and, on the face of it, practically normal geniculate input. This seemed to exonerate both the eye and the geniculate as primary sites of the damage and placed the main abnormality in the cortex. When we looked at the cortex histologically, we saw absolutely nothing to suggest any abnormality.
As we will see, the cortex does show anatomical defects, but they do not show up with these staining methods.
We next asked what it was about the eye closures that produced the abnormality. Closing the eye reduces the light reaching the retina by a factor of about ten to fifty; of course, it also prevents any images from reaching the retina. Could it be simply the reduction in light that was causing the trouble?
To help decide, we inserted in one eye of a newborn kitten an opalescent contact lens made of a plastic with the consistency of a ping pong ball. In some animals we instead surgically sewed over one eye a thin, translucent, opalescent membrane, in effect, an extra eyelid called the nictitating membrane that cats possess and we don't. The plastic or the membrane reduced the light by about one-half but prevented the formation of any focused images. The results were the same: an abnormal cortical physiology; an abnormal geniculate histology. Evidently it was the form deprivation rather than light deprivation that was doing the damage.
In a few kittens we tested vision before recording by putting an opaque black contact lens over the eye that had not been closed and then observing how the animal made out. The animals were clearly blind in the eye that had been deprived: they would walk confidently over to the edge of a low table, go past the edge, and fall to a mattress placed on the floor. On the floor they would walk into table legs. These are things no normal, self-respecting cat ever does. Similar tests with the eye that had not been closed showed that vision was entirely normal.
Next we did a protracted study in both cats and monkeys to learn whether the age at which the closures were done and the duration of the closures were important. It soon became clear that age of onset of deprivation was critical.
An adult cat deprived of vision in one eye for over a year developed no blindness in that eye, no loss of responses in the cortex, and no geniculate pathology. (The first cat we deprived, the mother of our first litter of kittens, was an
Abnormal layers appear in the left and right lateral geniculate bodies (seen in cross section) of a monkey whose right eye was closed at age two weeks for eighteen months. On both sides, the layers receiving input from the eye that was closed (the right eye) are paler: layers 1, 4, and 6 on the left; layers 2, 3, and 5 on the right, numbered from below. The cells in the affected layers are smaller, but this cannot be seen at such low power. The width of the entire structure is about 5 millimeters.
The lateral geniculate bodies of a kitten show obvious abnormalities when the right eye has been closed at ten days for thrceand-a-half months. The two main layers can be seen in the top half of the photographs. Top; In the left geniculate the upper layer (contralateral to the closed, right eye) is shrivelled and pale staining.
Bottom: In the right geniculate the lower of the two layers (ipsilateral) is abnormal. The two layers together are about 1 millimeter thick. The ocular-dominance histogram is shown at the top of this page..
A kitten (top histograms) was visually deprived after having its right eye closed at about ten days, the time at which the eyes normally open. The duration of closure was two-and-a-half months. In this experiment we recorded from only twenty-five cells. (In subsequent experiments we were able to record more cells, and we found a small percentage that were influenced from the eye that had been closed.) The results were very similar for a baby monkey (bottom histograms). It had its right eye closed at two weeks, and the eye remained closed for eighteen months. We subsequently found that the result is the same if the eye is closed tor only a few weeks.