The Mind and the Brain (16 page)

Synapses are pruned even more ruthlessly. Spinal cord synapses begin forming by the fifth week of embryogenesis, cortical synapses are forming at seven weeks, and
synaptogenesis
(synapse formation) continues through gestation and well into childhood. By one count, each cortical neuron forms, at the height of synaptogenesis, 15,000 connections: that works out to 1.8 million synapses per second from the second month in utero to the child’s second birthday. Which synapses remain, and which wither away, depends on whether they carry any traffic. If they do not, then like bus routes that attract no customers, they go out of business. By one estimate, approximately 20 billion synapses are pruned every day between childhood and early adolescence. It’s survival of the busiest. Like a cable TV subscription canceled because nobody’s watching, synaptic connections that aren’t used weaken and vanish. Here is where the power of genes falls off rapidly: genes may lead neurons to make their initial, tentative connections and control the order in which different regions of the brain (and thus physical and mental capacities) come on line, but it’s the environmental inputs acting on the plasticity of the young nervous system that truly determine the circuits that will power the brain. Thus, from the earliest stages of development, laying down brain circuits is an active rather than a passive process, directed by the interaction between experience and the environment. The basic principle is this: genetic signals play a large role in the initial structuring of the brain. The ultimate shape of the brain, however, is the outcome of an ongoing active process that occurs where lived experience meets both the inner and the outer environment. As we will see, as the prefrontal circuitry
matures, volitional choice can become a critical element in shaping the architecture bequeathed by both genetic factors and environmental happenstance.

Although the gross appearance and morphology of the brain change little after birth, neuroplasticity allows it to undergo immense changes at the cellular level, changes that underlie the unfolding cognitive and other capacities of a child. One of the starkest demonstrations of this has come from studies of speech perception. Newborns can hear all the sounds of the global Babel: the French
u
in
du
, the Spanish
n
, the English
th
. When one of the sounds stimulates hairs in the cochlea, the sound becomes translated into an electrical impulse that finds its way to the brain’s auditory cortex. As a racer hands off the baton in a relay, each neuron between ear and cortex passes the electrical impulse to the neuron beyond. After enough repetitions of a sound, the synapses connecting all those neurons have been strengthened just as Hebb described. The result is that this precise neuronal pathway responds to
th
every time, culminating in the stimulation of a dedicated cluster of neurons in the auditory cortex that produces the subjective sense that you have heard the sound
th
. The result is that networks of cells become tuned to particular sounds in the language the newborn constantly hears.

Space in the auditory cortex is limited, of course. Once the Hebbian process has claimed circuits, they are hard-wired for that sound; so far, neuroscientists have not observed any situations in which the Hebbian process is reversed so that someone born into a sea of, say, Finnish loses the ability to hear Finnish’s unique sounds. Although a growing appreciation of the plasticity of the adult brain has now overturned the idea that it is impossible to learn a second language and speak it without an accent after the age of twelve, without special interventions the auditory cortex is like development in a close-in suburb: it’s all built up, and there are no empty lots that can be dedicated to hearing new sounds.

Patricia Kuhl, a leading authority in speech development, got a
dramatic demonstration of this. In order to test Japanese adults and children on their ability to distinguish various phonemes, she made an audio disk with the various sounds and took it with her during a visit to the language lab of colleagues in Tokyo. Before testing any volunteers, she first wanted to demonstrate the disk to the Japanese scientists. As “rake, rake, rake” intoned through the high-end Yamaha speaker, her colleagues leaned forward expectantly for the sound change she had told them was coming. The disk segued into “lake, lake, lake,” Kuhl had said—but the Japanese, all proficient at English, still leaned in expectantly. They literally could not hear any difference between the sound of
lake
and the sound of
rake
.

The difference lay in their brains. Children who grow up hearing the sounds of a language form dedicated circuits in their auditory cortex: the brains of the children Kuhl left behind in Seattle, where she is a professor at the University of Washington, had been molded by their auditory experience to discriminate
r
from
l
. When? The seven-month-old Japanese babies whom Kuhl tested had no trouble discriminating
r
from
l
. But ten-month-olds were as deaf to the difference as adults. When Kuhl did a similar test of Canadian babies raised in English-speaking homes, she got the same results: six-month-olds could distinguish Hindi speech sounds even though those sounds were not part of their auditory world; by twelve months they could not. Between six and twelve months, Kuhl concludes, babies’ brains begin the “use it or lose it” process of pruning unused synapses. The auditory cortex loses its sensitivity to phonemes that it does not hear every day. This may be why children who do not learn a second language before puberty rarely learn to speak it like natives.

The reverse is true, too: connections that are used become stronger, even permanent elements of the neural circuitry. A newborn forms millions of connections every day. Everything he sees, hears, feels, tastes, and smells has the potential to shape the nascent circuits of his brain. The brain is literally wired by experience, with
sights, sounds, feelings, and thoughts leaving a sort of neural trace on the circuits of the cortex so that future sights, sounds, feeling, thoughts, and other inputs and mental activity are experienced differently than they would otherwise be. In the case of Kuhl’s young subjects, she speculates, the phonemes a child hears strengthen the auditory synapses dedicated to that sound; repeatedly hearing the sound broadens a child’s perceptual category for that sound, crowding out sounds with a similar auditory profile, until the number of auditory neurons dedicated to those neighboring sounds eventually dwindles to literally zero.

Clearly, the hardware of the brain is far from fixed at birth. Instead, it is dynamic and malleable. As far back as the 1960s and 1970s, researchers were documenting that rats raised in a lab cage with wheels to run on and ladders to scamper up, as well as other rats to interact with, grew denser synaptic connections and thicker cortices than rats raised with neither playmates nor toys. The “enriched” environment was closer to the world a rat would experience in the wilds of New York City, for example. The cortical differences translated into functional differences: rats with the thicker, more synaptically dense cortices mastered mazes and found hidden food more quickly than did rats from the poorer environments, who had thinner cortices.

From the moment a baby’s rudimentary sensory systems are operational (which for hearing and tactile stimulation occurs before birth), experiences from the world beyond begin to impinge on the brain and cause brain neurons to fire. Let’s return to the example of the visual system, which, when we left it, had axons from retinal neurons projecting into the nascent visual cortex. Alone among the senses, the visual system receives no stimulation until after birth. In the fourth week of gestation the eye begins to form. Synapses form first in the retina, then in subcortical visual areas, followed by the primary visual cortex, and, finally, higher visual centers in the temporal and parietal lobes. In the second trimester, the visual system experiences its growth spurt: between fourteen and twenty-eight
weeks, all of the 100 million neurons of the primary visual cortex form. They start to make synapses in the fifth month and continue making them for another year at the staggering rate of 10 billion per day, until the visual cortex reaches its maximal density at eight months of age. At birth, a baby sees the world through a glass darkly. More synapses responsible for processing motion than for perceiving form have come on line, with the result that babies detect movement better than they do shape. The entire visual field, in fact, consists of no more than a narrow tunnel centered on the line of sight, and the baby’s visual resolution is about one-fortieth that of a normal adult. Making the world look even odder (not that the baby has much to compare it to), newborns lack depth perception. They can see clearly only eight or so inches out. Normally, however, vision improves by leaps and bounds in the first few weeks, and by four months the baby can perceive stereoscopic depth. By six months, visual acuity has improved fivefold, and color vision, acuity, and volitional control of eye movements have all emerged. The tunnel of view expands, until by twelve months it is equivalent to an adult’s. Around a child’s first birthday, he sees the world almost as well as a normal adult.

The accurate wiring of the visual cortex that underlies the gradual improvement in vision occurs only if the baby receives normal visual stimuli. In other words, it is electrical activity generated by the very act of seeing that completes the wiring of the visual cortex. Again, although genes have played matchmaker between axons and neurons so that webs of neurons take shape, the number of human genes falls well short of the number needed to specify each synapse even within the visual cortex. Genes get the neurons to the right city and dispatch their axons to the general vicinity of neurons with which they will form synapses, but the baby’s unique interaction with the environment has to take it from there. Scientists concluded in the 1990s that one of the main ways axons and dendrites make connections—and neurons therefore form circuits—is by firing electrical signals, almost at random, and then precisely honing
the crude pattern to fit the demands of experience. “Even before the brain is exposed to the world, it is working to wire itself,” says the neuroscientist Carla Shatz, one of the pioneers in the field of brain development. She became a neuroscientist because, while she was in high school, her grandmother suffered a debilitating stroke that paralyzed one side of her body; Shatz vowed to join the search for how the nervous system works and settled on developmental neuroscience. “The adult pattern of connections emerges as axons remodel by the selective withdrawal and growth of different branches,” she says. “Axons apparently grow to many different addresses within their target structures and then somehow eliminate addressing errors.”

That “somehow” remains a holy grail of developmental neuroscience. Axons seem to be fairly promiscuous in their choice of target neurons: any will do. But then competition among inputs sorts out the axons, leading to areas with specific functions. An early clue to how they manage this feat came in the 1970s. David Hubel and Torsten Wiesel, working at Harvard, hit on the simple experiment of depriving newborn cats of visual input by sewing shut one of their eyes. After even a week of sightlessness, axons from the lateral geniculate nucleus representing the closed eye occupied a much smaller area of the cortex than did axons representing the normal eye. Then the scientists opened the eye that had been sewed shut, so that both eyes would deliver (it was thought) equal stimuli to the brain. They recorded from neurons in the primary visual cortex of the kittens, who by this time were at least four months old. Despite the fact that both eyes were open, virtually all of the visual cortex received input only from the eye that had been open since the kitten’s birth. Neurons from the eye that had been sewed shut formed few functional connections; it was as if the synapses had melted away from disuse. If kittens do not receive visual input between thirty and eighty days after birth (a window of time now known as the critical period), it is too late: the unused eye is blind forever. The development of visual function in the cortex depends on visual
inputs; visual deprivation early in life changes the cortex, Hubel and Wiesel found. Their work won them the 1981 Nobel Prize in physiology or medicine.

Extra activity—the opposite of deprivation—also changes the cortex, found the Harvard team. Brain regions stimulated by a kitten’s normal, open eye invaded and colonized regions that should have handled input from its closed eye. As a result, input from the normal eye reached a disproportionately large number of neurons in the visual cortex. Rather than the eyes’ having equal representation, most of the cortical cells received input only from the normal eye. This eye was now driving cells usually devoted to the shut eye. Yet this was not the case when the scientists recorded from cells in the retina or the lateral geniculate nucleus. That is, areas that should respond to stimulus of the normal eye did so, and areas that should respond to stimulus of the once-closed eye did not. Apparently, the majority of the changes induced by depriving the brain of visual input occurred in the cortex, not earlier in the visual pathway. This discovery suggested that if axons are carrying abnormally high electrical traffic, they take over more space in the visual cortex.

Other experiences produce even curiouser changes in the cortex. Neurons in the visual cortex turn out to be specialists. Some respond best to the sight of an edge oriented vertically, others to an edge oriented horizontally. There are roughly equal numbers of cells that respond to each orientation. But if the world of a newborn cat is skewed so that it sees only vertical lines, then in time most of its neurons will respond only to vertical edges. When a kitten is reared in a room painted with vertical stripes, very few of its direction-sensitive neurons turn out to specialize in horizontal stripes, but there is a profusion of vertical specialists. The animal literally cannot see horizontal lines but perceives vertical ones with great acuity. Human brains bear similar marks of early visual experience: a 1973 study found that Canadian Indians, growing up in teepees, had better visual acuity for diagonal orientations than peo
ple reared in the modern Western standard of horizontal ceiling joints and vertical wall joints.