Capacity of neurons and neural networks in the brain to change their connections and behaviour in response to new information, sensory stimulation, development, damage, or dysfunction. Rapid change or reorganization of the brain's cellular or neural networks can take place in many different forms and under many different circumstances. Neuroplasticity occurs when neurons in the brain sprout and form synapses. As the brain processes sensory information, frequently used synapses are strengthened while unused synapses weaken. Eventually, unused synapses are eliminated completely in a process known as synaptic pruning, which leaves behind efficient networks of neural connections. Neuroplasticity occurs during development in childhood, following physical injury such as loss of a limb or sense organ, and during reinforcement of sensory information such as in learning. Neuroplasticity forms the basis of research into brain-computer interface technology, in which computers are designed to interact with the brain to restore sensation in people with an impaired sense such as the loss of vision. Research on neuroplasticity is also aimed at improving scientists' understanding of how to reactivate or deactivate damaged areas of the brain in people affected by stroke, emotional disorders, chronic pain, psychopathy, or social phobia; such research may lead to improved treatments for these conditions.
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The concept of neuroplasticity pushes the boundaries of the brain areas that are still re-wiring in response to changes in environment. Several decades ago, the consensus was that lower brain and neocortical areas were immutable after development, whereas areas related to memory formation, such as the hippocampus and dentate gyrus, where new neurons continue to be produced into adulthood, were highly plastic. Hubel and Wiesel had demonstrated that ocular dominance columns in the lowest neocortical visual area, V1, were largely immutable after the critical period in development. Critical periods also were studied with respect to language; the resulting data suggested that sensory pathways were fixed after the critical period. However, studies determined that environmental changes could alter behavior and cognition by modifying connections between existing neurons and via neurogenesis in the hippocampus and other parts of the brain, including the cerebellum.
Decades of research have now shown that substantial changes occur in the lowest neocortical processing areas, and that these changes can profoundly alter the pattern of neuronal activation in response to experience. According to the theory of neuroplasticity, thinking, learning, and acting actually change both the brain's physical structure, or anatomy, and functional organization, or physiology from top to bottom. Neuroscientists are presently engaged in a reconciliation of critical period studies demonstrating the immutability of the brain after development with the new findings on neuroplasticity which reveal the mutability of both structural and functional aspects. A substantial paradigm shift is now under way: Canadian psychiatrist Norman Doidge has in fact stated that neuroplasticity is "one of the most extraordinary discoveries of the twentieth century."
In the late 1970s and early 1980s, several groups began exploring the impacts of removing portions of the sensory inputs. Michael Merzenich and Jon Kaas used the cortical map as their dependent variable. They found—and this has been since corroborated by a wide range of labs—that if the cortical map is deprived of its input it will become activated at a later time in response to other, usually adjacent inputs. At least in the somatic sensory system, in which this phenomenon has been most thoroughly investigated, JT Wall and J Xu have traced the mechanisms underlying this plasticity. Re-organization is not cortically emergent, but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex..
Merzenich and William Jenkins (1990) initiated studies relating sensory experience, without pathological perturbation, to cortically observed plasticity in the primate somatosensory system, with the finding that sensory sites activated in an attended operant behavior increase in their cortical representation. Shortly thereafter, Ford Ebner and colleagues (1994) made similar efforts in the rodent whisker barrel cortex (also somatic sensory system). These two groups largely diverged over the years. The rodent whisker barrel efforts became a focus for Ebner, Matthew Diamond, Michael Armstrong-James, Robert Sachdev, Kevin Fox, and Dan Feldman, and great inroads were made in identifying the locus of change as being at cortical synapses expressing NMDA receptors, and in implicating cholinergic inputs as necessary for normal expression. However, the rodent studies were poorly focused on the behavioral end, and Ron Frostig and Daniel Polley (1999, 2004) identified behavioral manipulations as causing a substantial impact on the cortical plasticity in that system.
Merzenich and DT Blake (2002, 2005, 2006) went on to use cortical implants to study the evolution of plasticity in both the somatosensory and auditory systems. Both systems show similar changes with respect to behavior. When a stimulus is cognitively associated with reinforcement, its cortical representation is strengthened and enlarged. In some cases, cortical representations can increase two to three fold in 1-2 days at the time at which a new sensory motor behavior is first acquired, and changes are largely finished within at most a few weeks. Control studies show that these changes are not caused by sensory experience alone: they require learning about the sensory experience, and are strongest for the stimuli that are associated with reward, and occur with equal ease in operant and classical conditioning behaviors.
An interesting phenomenon involving cortical maps is the incidence of phantom limbs. This is most commonly described in people that have undergone amputations in hands, arms, and legs, but it is not limited to extremities. The phantom limb feeling, which is thought to result from disorganization in the brain map and the inability to receive input from the targeted area, may be annoying or painful. Incidentally, it is more common after unexpected losses than planned amputations. There is a high correlation with the extent of physical remapping and the extent of phantom pain. As it fades, it is a fascinating functional example of new neural connections in the human adult brain.
The concept of plasticity can be applied to molecular as well as to environmental events The phenomenon itself is complex and can involve many levels of organization. To some extent the term itself has lost its explanatory value because almost any changes in brain activity can be attributed to some sort of "plasticity". For example, the term is used prevalently in studies of axon guidance during development, short-term visual adaptation to motion or contours, maturation of cortical maps, recovery after amputation or stroke, and changes that occur in normal learning in the adult.
Norman Doidge, following the lead of Michael Merzenich, separates manifestations of neuroplasticity into adaptations that have positive or negative behavioral consequences. For example, if an organism can recover after a stroke to normal levels of performance, that adaptiveness could be considered an example of "positive plasticity". An excessive level of neuronal growth leading to spasticity or tonic paralysis, or an excessive release of neurotransmitters in response to injury which could kill nerve cells; this would have to be considered a "negative" plasticity. In addition, drug addiction and obsessive-compulsive disorder are deemed examples of "negative plasticity" by Dr. Doidge, as the synaptic rewiring resulting in these behaviors is also highly maladaptive.
The adult brain is not "hard-wired" with fixed and immutable neuronal circuits. There are many instances of cortical and subcortical rewiring of neuronal circuits in response to training as well as in response to injury. There is solid evidence that neurogenesis, the formation of new nerve cells, occurs in the adult, mammalian brain--and such changes can persist well into old age. The evidence for neurogenesis is mainly restricted to the hippocampus and olfactory bulb, but current research has revealed that other parts of the brain, including the cerebellum, may be involved as well. In the rest of the brain, neurons can die, but they cannot be created. However, there is now ample evidence for the active, experience-dependent re-organization of the synaptic networks of the brain involving multiple inter-related structures including the cerebral cortex. The specific details of how this process occurs at the molecular and ultrastructural levels are topics of active neuroscience research. The manner in which experience can influence the synaptic organization of the brain is also the basis for a number of theories of brain function including the general theory of mind and epistemology referred to as Neural Darwinism and developed by immunologist Nobel laureate Gerald Edelman. The concept of neuroplasticity is also central to theories of memory and learning that are associated with experience-driven alteration of synaptic structure and function in studies of classical conditioning in invertebrate animal models such as Aplysia. This latter program of neuroscience research has emanated from the ground-breaking work of another Nobel laureate, Eric Kandel, and his colleagues at Columbia University College of Physicians and Surgeons.