CONCLUSION

About one hundred years ago, Santiago Ramón y Cajal, the father of modern neuroscience, stated that the adult brain is “fixed” and “immutable,” and this quickly became a central dogma of the field. Cajal’s own views about the brain’s capacity for plasticity are, however, ambiguous, and in fact he followed this famously pessimistic statement by remarking that “it is for the science of the future to change, if possible, this harsh decree.”

Neuroplasticity as We Know It

As we have seen in the preceding chapters, subsequent generations of neuroscientists have indeed changed the decree, by demonstrating numerous ways in which brain structure and function can change. Far from being fixed, the brain is a highly dynamic structure, which undergoes significant change not only as it develops but also throughout the entire lifespan. Neuroplasticity simply means change in the nervous system, and is a collective term for all the processes that change the structure and function of the brain. Brains evolved to respond and adapt to the environment, and so neuroplasticity is an intrinsic property of nervous tissue, which occurs at all levels of organization, from the genetic to the behavioral.

Far from being fixed, the brain is a highly dynamic structure, which undergoes significant change, not only as it develops, but also throughout the entire lifespan.

The mechanisms of neuroplasticity are extremely diverse, encompassing changes in the electrical properties of neurons that last just a few milliseconds, and large-scale structural changes that develop gradually over months and years. Some modes of plasticity occur continuously, such as the strengthening, weakening, creation, and elimination of synapses; these changes are thought to be critical for learning and memory. Others are employed at specific times and places, or under special circumstances—neurogenesis occurs extensively during development but is severely restricted in adults, whereas major cortical reorganization usually occurs only as a consequence of extensive training or nerve injury. The same mechanisms can have different effects, depending on when and where they are taking place; similarly, a given effect could be brought about by different mechanisms or combinations of them.

The various types of plasticity can act separately and in concert, and each is employed in specific brain areas at certain times—and whenever else it might be needed—to ensure proper brain development, maintain normal everyday brain function, and adapt to the environment through learning and experience. As a general rule, though, the capacity for plasticity decreases with age. The brain is most malleable during development and in early childhood, when it is highly sensitive to environmental stimuli of all kinds; that malleability decreases with age, making it progressively harder to learn. This helps to explain why a 6-year-old child can go on to lead a perfectly normal life after having an entire brain hemisphere removed, but an adult cannot, and why children who learned a language (or musicians who learned to play an instrument) at a young age have more pronounced structural changes than those who learned later.¹

Among the general public, the idea of neuroplasticity is viewed positively, and some people ascribe to it near-magical healing powers … [but] neuroplasticity is not a miracle cure that will heal any ailment, transform your life, or offer infinite potential for change.

Among the general public, the idea of neuroplasticity is viewed positively, and some people ascribe to it near-magical healing powers. It is because of plasticity that we are able to acquire new knowledge and skills and to recover, at least to some extent, from devastating brain injuries. Although we are beginning to learn how to enhance plasticity to facilitate recovery, this work is still in its early experimental stages, and the treatments developed thus far confer only modest benefits, if any. And neuroplasticity, although still not fully understood, must surely have limits within the physical constraints of its neurological substrates.

Neuroplasticity is not a miracle cure that will heal any ailment, transform your life, or offer infinite potential for change. It can also have negative consequences. Addiction can be thought of as a maladaptive form of learning, involving the modification of synapses within the brain’s reward and motivation circuits. Likewise, synaptic modifications in the pain pathway are responsible for certain chronic pain conditions. And the prolonged period of heightened plasticity that occurs in adolescence, while vital for maturation of the prefrontal cortex, also makes teens more vulnerable to addiction and mental illness.

Novel Forms of Neuroplasticity

The human brain is, as the cliché goes, the most complex object in the known universe. As such, it does not yield its secrets easily, so our understanding of neuroplasticity, and of brain function in general, is still very poor. Even as they struggle to understand the known forms of neuroplasticity, investigators continue to stumble upon novel mechanisms, some of which defy our long-held assumptions about how the brain works.

Take myelin, for example—the fatty tissue produced by oligodendrocytes in the brain and by Schwann cells in the peripheral nervous system. Each brain oligodendrocyte has a few extensions that form a large flat sheet of myelin, each of which wraps itself around a short segment of a single axonal fiber. Individual axons in the brain are thus insulated by numerous short segments of myelin, originating from many different oligodendrocytes and separated by the tiny lengths of bare fiber called nodes of Ranvier. This arrangement speeds up the conduction of nervous impulses along the fiber, by allowing them to jump from one node to another.²

Myelin is critical for the conduction of nervous impulses in the brain—as is evident from the devastation caused by multiple sclerosis and polio, both of which involve myelin degeneration. Given its importance, the distribution of myelin throughout the brain is thought to be highly stable. We have seen that neural pathways can be strengthened, and new ones created, in response to extensive training or serious injuries such as stroke; both processes involve the addition of newly formed myelin, but this happens gradually over weeks, months, or even longer periods.

A growing body of animal research now suggests that myelin redistribution can take place on much shorter timescales, however. For example, briefly training adult mice to run on a rotating wheel temporarily accelerates the production of oligodendrocytes in the brain, and blocking this new cell growth prevents the animals from mastering the new skill.³ Other recent research shows that neurotransmitter release regulates the number of myelin sheaths formed by individual oligodendrocytes, and that oligodendrocytes preferentially wrap newly formed myelin around electrically active axons, suggesting that myelin can be redistributed in an activity-dependent manner. Short-term changes in myelin distribution could affect the extent of synchronicity between distant brain regions—a property that is increasingly regarded as an important aspect of information processing.^4,5

Researchers continue to debate how many different types of neurons there are in the brain, and the cell types are classified in various ways, but there is general agreement that once a brain cell has matured, its identity remains fixed. Research published in the past few years, however, shows that neuronal identity can change, too. It’s thought that most neurons synthesize and release just one neurochemical transmitter, and so they can be classified as “dopaminergic,” “GABAergic,” or “glutamatergic,” according to which one they use. But it is now clear that at least some neurons can use more than one transmitter and, more surprisingly, that mature neurons can switch the transmitter they use, converting their excitatory synapses into inhibitory ones, or vice versa.⁶

Neurons can also be classified according to their electrical properties. For example, basket cells, the interneurons that control closure of the critical period in the visual cortex, are believed to exist in as many as 20 different types, the best known being the “fast-spiking” and “slow-spiking” ones, characterized according to the time frames of their responses. But it turns out that these cells can switch back and forth between fast- and slow-spiking activity, in response to neuronal activity. They appear to be constantly tuned in to neuronal network activity, and to change their firing properties in response by means of a protein that enters the nucleus and regulates the expression of potassium channels, which determine the cell’s firing rate. This suggests that the 20 apparently different types basket cells are actually one and the same, and that they morph along a continuum in an activity-dependent manner. Basket cells form networks that modulate neuronal network activity, and so this identity-switching mechanism could significantly impact neuronal population dynamics by altering the ratio of fast- to slow-spiking cells within a given network of neurons.⁷

Because of this diversity of mechanisms, neuroscientists still have not fully defined neuroplasticity, and as yet there is no general theory for it. So, many questions remain. For example, are different types of plasticity somehow linked by common underlying mechanisms, so that any given experience induces a set of related changes across multiple levels of organization? Or are there situations in which a particular type of plasticity can occur independently of others? Such questions are difficult to answer, because while researchers can use microscopes to examine cellular changes in the brains of experimental animals, and neuroimaging to visualize large-scale structural changes in humans, they cannot (so far) simultaneously analyze changes at multiple organizational levels.⁸

Ultimately, neuroscientists hope to bridge the chasm between molecular events and behaviors and thought processes, and to understand how they relate to one another. The brain is increasingly viewed as one vast network containing several hundred richly interconnected “hubs,” and huge amounts of money and effort are now being spent mapping brain connectivity at multiple scales. At smaller scales, brain connectivity appears to be constantly changing, but at larger scales it appears much more stable. But as we have seen, even apparently stable structures, such as long-range white matter tracts, are subject to changes that occur over longer time periods.⁹

Neuroplasticity therefore poses something of a challenge to those mapping brain connectivity, because it is still not clear exactly which types of changes are most closely correlated to our behaviors—or which scale of connectivity would be the most useful to map. Furthermore, although many similarities exist between the brains of individuals, there are also important differences. This is likely true of neuroplasticity, too: individual brains may differ in their capacity for plastic changes, so that the same experiences could induce different extents of neuroplasticity, and different types of plastic changes, in different people.

Thus, although the neuroplastic changes that occur in response to losing one’s sense of sight or hearing are well documented (see chapter 1), researchers occasionally describe patients in whom they do not occur. For example, a team of psychologists in the United States recently described the case of a patient known as M.M., who had been blind between the ages of 3 and 46 years. In 2000, he underwent a corneal transplant and stem cell surgery, which restored vision in one of his eyes. Tests carried out in the two years following surgery revealed that he still had severe amblyopia, however, and a decade later his ability to recognize objects and faces remained severely impaired.¹⁰

In fact, the structural and functional differences between individual brains probably outweigh their similarities. It’s very likely that no two brains are alike and, therefore, that there is no such thing as a “textbook brain.” Your brain is, to a large extent, unique, custom-built from the life experiences you have had since being in your mother’s womb, to meet the demands you place on it today. Neuroplasticity therefore lies at the heart of what makes us human, and of what makes each of us different from everyone else.