One obvious way to decide between these alternatives is to address
the question head on and simply record from a newborn cat or monkey. If
learning is necessary for the wiring up to occur, then we should fail to
find any of the rich specificity that we see in adult animals. A lack of specificity
would nevertheless not decide the issue, because we could then ascribe the
lack of connections either to immaturity—still-incomplete genetically
programmed wiring—or to lack of experience. On the other hand, finding such
specificity would argue against a learning mechanism. We did not expect the experiments with kittens to be easy, and they weren't. Kittens arc visually very
immature at birth and make no use at all of their eyes before about the tenth day,
when the eyes open. At that time, even the media of the eye, the transparent
substances between the cornea and the retina, are far from clear, so that it is
impossible to get a clear image on the retina. The immature visual cortex indeed responded sluggishly and somewhat unpredictably and was on the whole a far cry
from a normal adult visual cortex; nevertheless we found many clearly orientationspecific cells. The more days that elapsed between birth and recording,
the more the cells behaved like adult cells: perhaps because the media were
clearer and the animal more robust but perhaps because learning had occurred.
Interpretations differed from one set of observers to another.
The most convincing evidence came from newborn monkeys. The day after it is born, a macaque monkey is visually remarkably mature: unlike a
newborn cat or human, it looks, follows objects, and takes a keen interest in
its surroundings. Consistent with this behavior, the cells in the neonate monkey's primary visual cortex seemed about as sharply orientation-tuned as in
the adult. The cells even showed precise, orderly sequences of orientation
shifts (see the graph on this page). We did see differences between newborn
and adult animals, but the system of receptive-field orientation, the hallmark
of striate cortical function, seemed to be well organized.
Compared with that of the newborn cat or human, the newborn macaque monkey's visual system may be mature, but it certainly differs anatomically from the visual system of the adult monkey. A Nissl-stained section
of cortex looks different: the layers are thinner and the cells packed closer.
As Simon LeVay first observed, even the total area of the striate cortex expands
by about 30 percent between birth and adulthood. If we stain the cortex by the
Golgi method or examine it under an electron microscope, the differences are
even more obvious: cells typically have a sparser dendritic tree and fewer
Given these differences, we would be surprised if the cortex at birth
behaved exactly as it does in an adult. On the other hand, dendrites and synapses
are still sparser and fewer a month before birth. The nature-nurture question
is whether postnatal development depends on experience or goes on even
after birth according to a built-in program. We still are not sure of the
answer, but from the relative normality of responses at birth, we can conclude that
the unresponsiveness of cortical cells after deprivation was mainly due
to a deterioration of connections that had been present at birth, not to a failure
to form because of lack of experience.
The second major question had to do with the cause of this deterioration.
At first glance, the answer seemed almost obvious. We supposed that the
deterioration came about through disuse, just as leg muscles atrophy if the
knee or ankle is immobilized in a cast. The geniculate-cell shrinkage was presumably closely related to postsynaptic atrophy, the cell shrinkage seen in
the lateral geniculates of adult animals or humans after an eye is removed. It turned
out that these assumptions were wrong. The assumptions had seemed so selfevident that I'm not sure we ever would have thought of designing an
experiment to test them. We were forced to change our minds only because we
did what seemed to us at the time an unnecessary experiment, for reasons
that I forget.
We sutured closed both eyes, first in a newborn cat and later in a newborn monkey. If the cortical unresponsiveness in the path from one eye arose
from disuse, sewing up both eyes should give double the defect: we should
find virtually no cells that responded to the left or to the right eye. To
our great surprise, the result was anything but unresponsive cells: we found a
cortex in which fully half the cells responded normally, one quarter responded
abnormally, and one quarter did not respond at all. We had to conclude that
you cannot predict the fate of a cortical cell when an eye is closed unless
you are told whether the other eye has been closed too. Close one eye, and the
cell is almost certain to lose its connections from that eye; close both, and
the chances are good that the control will be preserved. Evidently we were dealing
not with disuse, but with some kind of eye competition. It was as if a cell
began by having two sets ofsynaptic inputs, one from each eye, and with one pathway not used, the other took over, preempting the territory of the first
pathway, as shown in the drawing below.
Such reasoning, we thought, could hardly apply to the geniculate shrinkage because geniculate cells are monocular, with no obvious opportunities
for competition. For the time being we could not explain the cell shrinkage
in the layers corresponding to the closed eye. With binocular closure, the
shrinkage of geniculate cells seemed less conspicuous, but it was hard to be sure
because we had no normal layers to use as a standard of comparison. Our understanding of this whole problem did not move ahead until we began to use some
of the new methods of experimental anatomy.