The story of how we grow and change across the life span is one of the most interesting in all of psychology. But as with any story, we must begin at the beginning, with a consideration of how genetic and environmental factors interact to shape us before we are even born.
The voyage toward becoming a human being begins at conception, when a sperm and egg cell unite to form the fertilized egg or zygote (Figure 14.1). Within hours of this union of sperm and egg, the nuclei of the two cells merge, creating a novel combination of 23 pairs of chromosomes, half from the mother and half from the father. The zygote begins a process of dividing and redividing, producing a blastocyst, a mass of identical cells.
About 10 to 14 days after fertilization, the blastocyst attaches itself to the wall of the uterus. Then, the embryonic stage begins (Figure 14.2). During this phase, critical genes turn on and produce chemical signals that induce a process of differentiation among the proliferating cells. The mass of cells (now called an embryo) soon has three distinct cell types—those that will become the nervous system and the outer skin; those that will form the skeletal system and voluntary muscles; and those that will form the gut and digestive organs.
One month after conception, the placenta and umbilical cord have developed, and the embryo begins to develop the major organ systems of the body (including the heart and lungs), as well as arms, legs, and facial features. At about this same time, we can detect the beginnings of a nervous system: a structure called a neural tube with three identifiable subparts, one that will develop into the brain stem and spinal cord, and two others that will develop into the midbrain and forebrain (Figure 14.3).
Two months after conception, the fetal stage begins. By this point, the mass of cells (now called a fetus) has grown to 1 inch in length and the heart has begun to beat. The nervous system continues to grow at a remarkable pace. New nerve cells are generated at a rate that can approach 250,000 new cells per minute (Kolb & Whishaw, 2009; Mueller, 1996), and these cells start to form themselves into a network. Several mecha-nisms contribute to this networking, including specific genes that produce chemical sig-nals that serve as “beacons,” attracting connections that sprout from other nerve cells.
Even at this early stage, the fetus is capable of simple behaviors, and so will show a sucking reflex if its lips are touched. It’s not long before other—more sophisticated— capacities come into view, including the capacity for learning. For example, in one now-classic study, DeCasper and Spence (1986) asked pregnant mothers to read aloud to their unborn infants twice a day for the last 6 weeks of their pregnancy from one of two Dr. Seuss books. Once the children were born, researchers set up an apparatus that was controlled by the way the newborns sucked on a special pacifier; if they sucked in one way, the apparatus played the story their mothers had read before they were born; if they sucked in another way, the apparatus played an unfamiliar story. The researchers found that infants adjusted their sucking pattern so that they could listen to the story to which they had been exposed in utero, indicating that the infants had “learned” one story and preferred it to the story they did not know.
A great deal of prenatal development is powerfully guided by the genome. Environmental factors are just as important, however, as we have seen in the capacity of the fetus to learn from its experiences. But what in general does “environment” mean in this early stage of development?
Consider the earliest stages of embryonic growth. Some of the cells in the embryo will eventually become the brain; others will become the gall bladder or the bones of the foot. But every cell in the embryo has the same genes, and so presumably all receive the same genetic instructions. How does each cell manage to develop appropriately?
The answer seems to be that the fate of each cell is determined in part by its cellular neighbors—the cells that form its physical environment. Evidence comes from studies of salamander embryos. Early in their development, salamanders have an outer layer of tissue that gradually differentiates, and cells in this layer will become teeth only if they make contact with certain other cells in the embryo’s mouth region. Without this contact, cells in this layer become skin.
In humans, the cells that will become the brain initially show no distinction between neurons and glia. As the cells reproduce and differentiate, though, these two types become distinct, and the newly created neurons actually migrate toward their appropriate posi-tions. This migration process is guided by glia that act as guidewires. Various chemicals also guide the process by attracting some types of nerve cells and repelling other types (Hatten, 2002). In all cases, the migrating neurons approach the surface of the develop-ing cortex, but the first-arriving neurons stop short of the surface. Later-arriving neurons pass these now-stationary cells, and these late arrivals in turn are passed by even later arrivals. As a result, the cortex literally develops from the inside out, with layers closer to the surface established later than deeper layers.
Of course, it’s not enough that the nerve cells end up in the right places; they also need to end up connected in the right way, so that each nerve cell sends its messages to the right target. How does each developing nerve cell come to know its eventual target? The answer, of course, begins with the genes. Early in development, genetic specifica- tions lead neurons to form protomaps, providing a rough “wiring diagram” for the brain’s circuits. The areas mapped in this way seem to attract connections from the appropriate inputs, so that, for example, the protomap in the projection area for vision attracts afferent fibers from the thalamus, with the result that the visual cortex comes to receive the right input signals (e.g., Rakic, 1995; for some complexities, though, see Sur & Rubenstein, 2005).
Inevitably, there are some wiring errors, but there is a safeguard in place to deal with these. Many more neurons are created than are needed, and each neuron tries to form far more connections than are required. If a neuron’s connections prove either wrong or redundant, that neuron can withdraw its connections and find better targets, or it can be given a message to die (Kuan, Roth, Flavell, & Rakic, 2000; Rubenstein & Rakic, 1999). In fact, it is normal for between 20 and 80% of neurons to die as the brain develops, depending upon the region of the brain. This decimation primarily occurs early in development—in humans, about 4 to 6 months after conception (Rosenzweig, Leiman, & Breedlove, 1996)—but according to some investigators, it continues at a slower rate for much longer, perhaps even a decade.
So far, we have focused on how the local environment surrounding each neuron guides its differentiation and migration. More global features of the environment also play a major role, namely, the organism’s own bodily fluids, especially its blood. Thus, for example, hormones circulating in the fetus’s blood have a powerful influence on the development of the child’s external anatomy, the development of the nervous system, and even later sex-typical play (Auyeung et al., 2009). Moreover, the bloodstream of mammalian embryos is intimately connected to the mother’s blood supply, and so her blood, too, becomes part of the embryo’s environment.
The maternal blood supplies oxygen and nutrition to the developing fetus, and this is one of the reasons why normal development depends on the nutritional state of the mother. But the mother’s blood supply also plays another role—it provides a conduit through which factors in the external environment can influence the fetus. Unfortunately, many of these external factors are teratogens—factors that can disrupt development. The long list of teratogens includes environmental toxins such as lead and mercury, as well as alcohol, cigarette smoke, X-rays, and diseases such as rubella (German measles). Teratogens can have a number of negative effects, depending on the type, timing, and amount of exposure. For example, when a pregnant woman drinks alcohol, the alcohol enters both her bloodstream and that of her fetus. Even light drink-ing can affect the brain of the developing fetus (Ikonomidou et al., 2000), and heavy drinking can lead to fetal alcohol syndrome, which is characterized by both psycholog-ical problems (learning disorders and behavior difficulties) and physical abnormalities (smaller stature and a characteristic pattern of facial abnormalities; Figure 14.4).
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