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 to the left). 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 
synapses. 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 
self-evident 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.