human brain does not contain any distinct anatomical structures or types of neurons associated with language. The human brain areas most crucial for language, Wernicke’s and Broca’s areas on the left side (in most humans), have homologous areas in other primates, but these areas do not support language. Yet all normal human infants learn, without any explicit instruction, whatever language to which they are exposed, but other animals do not learn grammatical, word-order based language despite extensive instruction.
The capacity for learning language is built in, but neuroscience does not now know how. One clue may be brain lateralization, however. Left- versus right-side specialization for some types of audio processing and production exists in other mammals, and even some birds, but is nowhere near as extensive as in humans.
A similar association exists with right-hand dominance, driven by the left side of the brain, which is more extensive in humans than any other animal. Chimpanzees, for example, may be relatively right- or left-hand preferring, but most have no overall tendency to be strongly right-handed or left-handed, the way humans do.
Neuroscience’s view of emotions has changed markedly in the last decades. Earlier views regarded emotions as leftovers from our evolution from non-rational species. Star Trek’s Mr. Spock could be taken as a model of a superior, more evolved humanoid. However, we now know that emotions are a means of nonverbal communication within our brains. Hunches and anxiety in certain situations are signs of danger and the need to be cautious.
We see the usefulness of this nonverbal information in people with damage to the orbitofrontal cortex or amygdala. They may gamble recklessly or commit social faux pas because they lack internal feelings about the mistakes they’re making.
Developmental, Neurological, and Mental Disorders and Treatments
One of the most important reasons to understand neurobiology is to understand mental disorders and treatments. The good news is that great progress is being made in this field now. We know the genetic bases of many developmental disorders, such as Fragile X and William’s syndrome. The bad news is that many disorders remain that we do not know about, and, even among disorders with known genetics, how the gene alteration produces the disorder, and what to do about it, are not clear. Chapters 15 through 18 discuss the background and current treatment approaches (if any) of many common neurological disorders.
Developing the brain and nervous system
The set of genes that define an organism is not a blueprint that is executed by a builder, but a set of procedures that brings about the development of the organism.
A useful metaphor is an ant hill or termite mound. No master ant or termite knows how to build a hill or mound and directs the other insects. Instead, ants and termites respond to each other, and to the environment, by digging holes and gluing arches together. Some holes and arches reach a critical mass that causes nearby insects to concentrate on those structures and related structures, which triggers the completion of the insect home as though its builders were following a design.
Developing cells have genetically coded responses to substances they detect by their membranes or ingest, including cell identity and brain location marker molecules. Cell responses include movement, division, and secretion of other markers and agents. The interactions among cells that have these responses in the embryological environment builds the brain.
Much of the genome is only expressed extensively during development, a time when the organism is also particularly susceptible to toxins that mimic or interfere with these markers and agents. The result of this interference is the construction of an improperly set-up brain, which is typically much worse than inferring temporarily with a properly constructed brain later in life, which often can be reversed.
Movement disorders and symptoms
Movement disorders can originate with brain damage that compromises the control of movement, or neurons that drive muscles, or the muscles themselves. Chapter 16 discusses some of the most common movement disorders. Cerebral palsy and epilepsy typically involve brain damage. Multiple sclerosis is caused by demyelination of axons of motor and other neurons. Myasthenia gravis is an autoimmune disease involving the cholinergic receptors on muscle cells.
Some well-known movement disorders, such as Parkinson’s and Huntington’s diseases, occur only later in life. Neither of these diseases is curable, but a number of treatments can partially alleviate the symptoms of Parkinson’s disease. Accidents involving brain or spinal trauma still produce many cases of paralysis every year. Extensive research efforts using stem cells, neural growth factors, and electrical stimulation continue to be made for these problems.
Neural dysfunctions and mental illness
The history of clinical thought on mental illness is a pendulum ride between organic and environmental causes. In the United States, particularly, the dominance of behaviorism in academic psychology and psychiatry was associated with behavioral and cognitive therapeutic strategies based on “undoing” some sort of bad environmental influence or improper response to a relatively normal environment.
Knowledge of genetics, neurotransmitter systems, and the development of neurotransmitter-analog drugs led to pharmacological treatments that were at least partially effective in many psychiatric patients for whom traditional therapy had provided no relief. Schizophrenia and autism are cases in point. In the mid 20th century, the detection of schizophrenia or autism often was treated by family therapy sessions around behavioral theories such as withdrawn, uncaring so-called “refrigerator mothers” being the cause of these disorders.
It is now clear that both schizophrenia and autism have high heritability, although environmental factors are undoubtedly important in the expression and outcome of the disorder. Pharmacological agents deal well with many of the positive symptoms of schizophrenia such as hallucinations. But both schizophrenia and autism have multiple genetic causes, and the relation between the genetic anomaly and the neural dysfunction leading to the phenotype are poorly known. This situation is unfortunately also the case with many other mental disorders, including depression.
Repair and enhancement with artificial brains
Humans increasingly are electronically connected to each other through computers, cellphones, and soon, wearable devices like watches and electronic eyeglasses. It may be a short time before some of this technology is implantable. Brain implants may allow people who are paralyzed to operate computers or control their own or prosthetic limbs.
Deep brain stimulation, originally used widely to relieve Parkinson’s disease symptoms, may also be effective in treating some types of depression. Transcranial magnetic stimulation may also mitigate depression without many of the side effects of electroconvulsive therapy (ECT, commonly referred to as “shock treatment”). Transcranial electrical stimulation has been shown in numerous studies to increase learning rates. A new term electroceuticals has been introduced for the field of electrical brain stimulation for therapeutic effect. Brain scientists live in exciting times!
Chapter 2
Building Neurons from Molecules
In This Chapter