The human brain is surprisingly imperfect. Far from being a single, elegant machine—the enchanted loom the philosophers wrote so poetically about—the human brain is instead a system comprised of many distinct components that have been added at different times during the course of evolution. The human species has retained what worked best in earlier versions of the brain, then added bits and pieces to get us to our present state through evolution.

To understand the central nervous system, it is helpful to consider two aspects of its development. Prenatal development (growth from conception to birth), reveals how the nervous system develops and changes within each member of a species. Evolutionary development reveals how the nervous system in humans evolved and adapted from other species.

The nervous system is the first major bodily system to take form in an embryo (Moore, 1977). It begins to develop within the 3rd week after fertilization, when the embryo is still in the shape of a sphere. Initially, a ridge forms on one side of the sphere and then builds up at its edges to become a deep groove. The ridges fold together and fuse to enclose the groove, forming a structure called the neural tube. The tail end of the neural tube will remain a tube, and as the embryo grows larger, it forms the basis of the spinal cord. The tube expands at the opposite end, so that by the 4th week the three basic levels of the brain are visible. During the 5th week, the forebrain and hindbrain further differentiate into subdivisions. During the 7th week and later, the forebrain expands considerably to form the cerebral hemispheres.

As the embryonic brain continues to grow, each subdivision folds onto the next one and begins to form the structures easily visible in the adult brain (see FIGURE 3.20). The hindbrain forms the cerebellum and medulla, the midbrain forms the tectum and the tegmentum, and the forebrain subdivides further, separating the thalamus and hypothalamus from the cerebral hemispheres. Over time, the cerebral hemispheres undergo the greatest development, ultimately covering almost all the other subdivisions of the brain.

The ontogeny of the brain (how it develops within a given individual) is pretty remarkable. In about half the time it takes you to complete a 15-week semester, the basic structures of the brain are in place and rapidly developing, eventually allowing a newborn to enter the world with a fairly sophisticated set of abilities. In comparison, the phylogeny of the brain (how it developed within a particular species) is a much slower process. However, it, too, has allowed humans to make the most of the available brain structures, enabling us to perform an incredible array of tasks.

The central nervous system evolved from the very simple one found in simple animals to the elaborate nervous system in humans today. Even the simplest animals have sensory neurons and motor neurons for responding to the environment (Shepherd, 1988). For example, single-celled protozoa have molecules in their cell membrane that are sensitive to food in the water. Those molecules trigger the movement of tiny threads called cilia, which help propel the protozoa toward the food source. The first neurons appeared in simple invertebrates, such as jellyfish; the sensory neurons in the jellyfish’s tentacles can feel the touch of a potentially dangerous predator, which prompts the jellyfish to swim to safety. If you are a jellyfish, this simple neural system is sufficient to keep you alive. The first central nervous system worthy of the name, though, appeared in flatworms. The flatworm has a collection of neurons in the head—a simple kind of brain—that includes sensory neurons for vision and taste and motor neurons that control feeding behaviour. Emerging from the brain is a pair of tracts that form a spinal cord.

During the course of evolution, a major split in the organization of the nervous system occurred between invertebrate animals (those without a spinal column) and vertebrate animals (those with a spinal column). In all vertebrates, the central nervous system is organized into a hierarchy: The lower levels of the brain and spinal cord execute simpler functions, while the higher levels of the nervous system perform more complex functions. As you saw earlier, in humans, reflexes are accomplished in the spinal cord. At the next level, the midbrain executes the more complex task of orienting toward an important stimulus in the environment. Finally, a more complex task, such as imagining what your life will be like 20 years from now, is performed in the forebrain (Addis, Wong, & Schacter, 2007; Schacter, Addis, et al., 2012; Szpunar, Watson, & McDermott, 2007).

The forebrain undergoes further evolutionary advances in vertebrates. In lower vertebrate species such as amphibians (frogs and newts), the forebrain consists only of small clusters of neurons at the end of the neural tube. In higher vertebrates, including reptiles, birds, and mammals, the forebrain is much larger, and it evolves in two different patterns. Reptiles and birds have almost no cerebral cortex. By contrast, mammals have a highly developed cerebral cortex, which develops multiple areas that serve a broad range of higher mental functions. This forebrain development has reached its peak—so far—in humans (FIGURE 3.21).

The human brain, then, is not so much one remarkable thing; rather, it is a succession of extensions from a quite serviceable foundation. Like other species, humans have a hindbrain, and as in those species, it performs important tasks to keep us alive. For some species, that is sufficient. All flatworms need to do to ensure their species’ survival is eat, reproduce, and stay alive a reasonable length of time. But as the human brain evolved, structures in the midbrain and forebrain developed to handle the increasingly complex demands of the environment. The forebrain of a bullfrog is about as differentiated as it needs to be to survive in a frog’s world. The human forebrain, however, shows substantial refinement, which allows for some remarkable, uniquely human abilities: self-awareness, sophisticated language use, abstract reasoning, and imagining, among others.

There is intriguing evidence that the human brain evolved more quickly than the brains of other species (Dorus et al., 2004). Researchers compared the sequences of 200 brain-related genes in mice, rats, monkeys, and humans and discovered a collection of genes that evolved more rapidly among primates. What is more, they found that primate brains not only evolved quickly compared to those of other species, but the brains of the particular primates who eventually became humans evolved even more rapidly. These results suggest that in addition to the normal adaptations that occur over the process of evolution, the genes for human brains took particular advantage of a variety of mutations (changes in a gene’s DNA) along the evolutionary pathway (Vallender, Mekel-Bobrov, & Lahn, 2008). These results also suggest that the human brain is still evolving—becoming bigger and more adapted to the demands of the environment (Evans et al., 2005; Mekel-Bobrov et al., 2005).

Genes may direct the development of the brain on a large, evolutionary scale, but they also guide the development of an individual and, generally, the development of a species. Let us take a brief look at how genes and the environment contribute to the biological bases of behaviour.

Is it genetics (nature) or the environment (nurture) that reigns supreme in directing a person’s behaviour? The emerging picture from current research is that both nature and nurture play a role in directing behaviour, and the focus has shifted to examining the interaction of the two rather than the absolute contributions of either alone (Gottesman & Hanson, 2005; Rutter & Silberg, 2002; Zhang & Meaney, 2010).

A gene is the major unit of hereditary transmission. Historically, the term gene has been used to refer to two distinct but related concepts. The initial, relatively abstract concept of a gene referred to units of inheritance that specify traits such as eye colour. More recently, genes have been defined as sections on a strand of DNA (deoxyribonucleic acid) that code for the protein molecules that affect traits. Genes are organized into large threads called chromosomes, strands of DNA wound around each other in a double-helix configuration (see FIGURE 3.22). The DNA in our chromosomes produces protein molecules through the action of a molecule known as messenger RNA (ribonucleic acid; mRNA), which communicates a copy of the DNA code to cells that produce proteins. Chromosomes come in pairs, and humans have 23 pairs each. These pairs of chromosomes are similar but not identical: You inherit one of each pair from your father and one from your mother. There is a twist, however: The selection of which of each pair is given to you is random.

Perhaps the most striking example of this random distribution is the determination of sex. In mammals, the chromosomes that determine sex are the X and Y chromosomes; females have two X chromosomes, whereas males have one X and one Y chromosome. You inherited an X chromosome from your mother because she has only X chromosomes to give. Your biological sex, therefore, was determined by whether you received an additional X chromosome or a Y chromosome from your father.

As a species, we share about 99 percent of the same DNA (and almost as much with other apes), but there is a portion of DNA that varies across individuals. Children share more of this variable portion of DNA with their parents than with more distant relatives or with nonrelatives: They share half their genes with each parent, a quarter of their genes with their grandparents, an eighth of their genes with cousins, and so on. The probability of sharing genes is called degree of relatedness. The most genetically related people are monozygotic twins (also called identical twins), who develop from the splitting of a single fertilized egg and therefore share 100 percent of their genes. Dizygotic twins (fraternal twins) develop from two separate fertilized eggs and share 50 percent of their genes, the same as any two siblings born separately.

Many researchers have tried to determine the relative influence of genetics on behaviour. One way to do this is to compare a trait shown by monozygotic twins with that same trait among dizygotic twins. This type of research usually enlists twins who were raised in the same household, so that the impact of their environment (their socioeconomic status, access to education, parental child-rearing practices, and environmental stressors) remains relatively constant. Finding that monozygotic twins have a higher presence of a specific trait suggests a genetic influence (Boomsma, Busjahn, & Peltonen, 2002).

As an example, the likelihood that the dizygotic twin of a person who has schizophrenia (a mental disorder we will discuss in greater detail in the Psychological Disorders chapter) will also develop schizophrenia is 27 percent. However, this statistic rises to 50 percent for monozygotic twins. This observation suggests a substantial genetic influence on the likelihood of developing schizophrenia. Monozygotic twins share 100 percent of their genes and, if one assumes environmental influences are relatively consistent for both members of the twin pair, the 50 percent likelihood can be traced to genetic factors. That sounds frighteningly high … until you realize that the remaining 50 percent probability must be due to environmental influences. In short, genetics can contribute to the development, likelihood, or onset of a variety of traits. But a more complete picture of genetic influences on behaviour must always take the environmental context into consideration. Genes express themselves within an environment, not in isolation.

The idea that genes are expressed within an environment is central to an important and rapidly growing area of research known as epigenetics: environmental influences that determine whether or not genes are expressed, or the degree to which they are expressed, without altering the basic DNA sequences that constitute the genes themselves. To understand how epigenetic influences work, it is useful to think about DNA as analogous to a script for a play or a movie. The biologist Nessa Carey (2012) offers the example of Shakespeare’s Romeo and Juliet, which was made into a movie back in 1936 starring classic actors Leslie Howard and Norma Shearer, and in 1996 starring Leonardo DiCaprio and Claire Danes. Shakespeare’s script formed the basis of both films, but the directors of the two films used the script in different ways, and the actors in the two films gave different performances. Thus, the final products departed from Shakespeare’s script and were different from one another, even though Shakespeare’s original script still exists. Something similar happens with epigenetics: Depending on the environment, a gene can be expressed or not without altering the underlying DNA code.

The environment can influence gene expression through epigenetic marks, chemical modifications to DNA that can turn genes on or off. You can think of epigenetic marks as analogous to notes that the movie directors made on Shakespeare’s script that determined how the script was used in a particular film. There are two widely studied epigenetic marks:

You may have wondered whether Claire Danes’s performance in Romeo and Juliet prepared her to play Carrie in Homeland (come to think of it, Carrie’s relationship with Brody bears some resemblance to Shakespeare’s doomed lovers). But what is the relevance of epigenetics to the brain and to psychology? It turns out to be more relevant than anyone suspected until the past decade or so. Experiments with rats and mice have shown that epigenetic marks left by DNA methylation and histone modifcation play a role in learning and memory (Bredy et al., 2007; Day & Sweatt, 2011; Levenson, & Sweatt, 2005). Several studies (including recent research with humans) have linked epigenetic changes with responses to stress (Zhang & Meaney, 2010). For example, studies of nurses working in high-stress versus low-stress environments found differences between the two groups in DNA methylation (Alasaari et al., 2012). Subjective levels of stress in a sample of 92 Canadian adults, as well as physiological signs of stress, were correlated with levels of DNA methylation (Lam et al., 2012). Another study reported a link between DNA methylation and early life experience, with differences observed between individuals who grew up in relatively affluent households versus those who grew up in poverty, even when controlling for such factors as current socioeconomic status (Lam et al., 2012). Similar findings were reported in a separate study of 40 British adults (Borghol et al., 2012). These observations fit well with an important line of research described in the Hot Science box, showing that DNA methylation and histone modifications play a key role in the long-lasting effects of early experiences for both rodents and humans.

Genes set the range of possibilities that can be observed in a population, but the characteristics of any individual within that range are determined by environmental factors and experience. The genetic capabilities that another species might enjoy, such as breathing underwater, are outside the range of your possibilities, no matter how much you might desire them.

With these parameters in mind, behavioural geneticists use calculations based on relatedness to compute the heritability of behaviours (Plomin et al., 2001). Heritability is a measure of the variability of behavioural traits among individuals that can be accounted for by genetic factors. Heritability is calculated as a proportion, and its numerical value (index) ranges from 0 to 1.00. A heritability of 0 means that genes do not contribute to individual differences in the behavioural trait; a heritability of 1.00 means that genes are the only reason for the individual differences. As you might guess, scores of 0 or 1.00 occur so infrequently that they serve more as theoretical limits than realistic values; almost nothing in human behaviour is completely due to the environment or owed completely to genetic inheritance. Scores between 0 and 1.00, then, indicate that individual differences are caused by varying degrees of genetic and environmental contributions—a little stronger influence of genetics here, a little stronger influence of the environment there, but each always within the context of the other (Moffitt, 2005; Zhang & Meaney, 2010).

For human behaviour, almost all estimates of heritability are in the moderate range, between 0.30 and 0.60. For example, a heritability index of 0.50 for intelligence indicates that half of the variability in intelligence test scores is attributable to genetic influences and the remaining half is due to environmental influences. Smart parents often (but not always) produce smart children; genetics certainly plays a role. But smart and not-so-smart children attend good or not-so-good schools, practise their piano lessons with more or less regularity, study or not study as hard as they might, have good and not-so-good teachers and role models, and so on. Genetics is only half the story in intelligence. Environmental influences also play a significant role in predicting the basis of intelligence (see the Intelligence chapter).

Heritability has proven to be a theoretically useful and statistically sound concept in helping scientists understand the relative genetic and environmental influences on behaviour. However, there are four important points about heritability to bear in mind. First, remember that heritability is an abstract concept: It tells us nothing about the specific genes that contribute to a trait. Second, heritability is a population concept: It tells us nothing about an individual. Heritability provides guidance for understanding differences across individuals in a population rather than abilities within an individual.

Third, heritability is dependent on the environment. Just as behaviour occurs within certain contexts, so do genetic influences. For example, intelligence is not an unchanging quality: People are intelligent within a particular learning context, a social setting, a family environment, a socioeconomic class, and so on. Heritability, therefore, is meaningful only for the environmental conditions in which it was computed, and heritability estimates may change dramatically under other environmental conditions. Finally, heritability is not fate. It tells us nothing about the degree to which interventions can change a behavioural trait. Heritability is useful for identifying behavioural traits that are influenced by genes, but it is not useful for determining how individuals will respond to particular environmental conditions or treatments.