Neuroplasticity

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Neuroplasticity (variously referred to as brain plasticity or cortical plasticity) refers to the changes that occur in the organization of the brain, and in particular changes that occur to the location of specific information processing functions, as a result of the effect of experience during development and as mature animals. A common and surprising consequence of brain plasticity is that the location of a given function can "move" from one location to another in the brain due to repeated learning or brain trauma. Neuroplasticity is a fundamental issue that supports the scientific basis for treatment of acquired brain injury with goal-directed experiential therapeutic programs in the context of rehabilitation approaches to the functional consequences of the injury.

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. Some authors separate forms into adaptations that have positive or negative consequences for the animal. For example, if an organism, after a stroke, can recover 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, would have to be considered perhaps as a "negative or maladaptive" plasticity.

The main thing to know is that even the adult brain is not "hard-wired" with fixed and immutable neuronal circuits. Many people have been taught to believe that once a brain injury occurs, there is little to do to repair the damage. This is simply not the case and there is no fixed period of time after which "plasticity" is blocked or lost. We simply do not know all of the conditions that can enhance neuronal plasticity in the intact and damaged brain, but new discoveries are being made all of the time. 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 restricted to the hippocampus and olfactory bulb. 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 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.

1 Brain plasticity and cortical maps
- 1.1 Related reading
2 Brain plasticity during operation of brain-machine interfaces
- 2.1 Related reading
3 General reading
4 See also
5 External links

[edit] Brain plasticity and cortical maps

Cortical organization, especially for the sensory systems, is often described in terms of maps. For example, sensory information from the foot projects to one cortical site and the projections from the hand target in another site. As the result of this somatotopic organization of sensory inputs to the cortex, cortical representation of the body resembles a map (or homunculus). Interestingly, cortical maps are not fixed, but rather plastic. In the late 1970s and early 1980s, several groups began exploring the impacts of removing portions of the sensory inputs. Merzenich and Kaas used the cortical map as their dependent measure. 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, Wall and Xu have traced the mechanisms underlying this plasticity. Re-organization occurs at every level in the processing hierarchy to result in the map changes observed in the cerebral cortex. It is not cortically emergent.

Merzenich and 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, Ebner and colleagues (1994) made similar efforts in the rodent whisker barrel (also somatic sensory system). These two groups largely diverged over the years. The rodent whisker barrel efforts became a focus for Ebner, Diamond, Armstrong-James, Sachdev, Fox, and 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 Frostig and Polley (1999,2004) identified behavioral manipulations as causing a substantial impact on the cortical plasticity in that system.

Merzenich and 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 with 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 homunculus 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.

[edit] Related reading

Ramachandran & Hirstein (1998). "The perception of phantom limbs", Brain, 121: 1603-1630.
Flor, H. (2002). "Phantom limb pain: Characteristics, causes, and treatments." Lancet Neurology, 1: 182-189.

[edit] Brain plasticity during operation of brain-machine interfaces

Brain-machine interface (BMI) is a rapidly developing field of Neuroscience. According to the results obtained by Mikhail Lebedev, Miguel Nicolelis and their colleagues (Lebedev et al. 2005), operation of BMIs results in incorporation of artificial actuators into brain representations. The scientists showed that modifications in neuronal representation of the monkey's hand and the actuator that was controlled by the monkey brain occurred in multiple cortical areas while the monkey operated a BMI. Initially, monkeys moved the actuator by pushing a joystick. After the monkey started using its brain activity to directly control the actuator, the activity of individual neurons and neuronal populations became less representative of the animal's hand movements while representing the movements of the actuator. Presumably as a result of this adaptation, the animals could eventually stop moving their hands yet continue to operate the actuator. Thus, during BMI control, cortical ensembles plastically adapt to represent behaviorally significant motor parameters, even if these are not associated with movements of the animal's own limb.

Active laboratory groups include those of John Donoghue at Brown, Richard Andersen at Caltech, Krishna Shenoy at Stanford, Nicholas Hatsopoulos of University of Chicago, Andy Schwartz at Pitt, Sandro Mussa-Ivaldi at Northwestern and Miguel Nicolelis at Duke. Donoghue and Nicolelis' groups have independently shown that animals can control external interfaces in tasks requiring feedback, with models based on activity of cortical neurons, and that animals can adaptively change their minds to make the models work better. Donoghue's group took the implants from Richard Normann's lab at Utah (the "Utah" array), and improved it by changing the insulation from polyimide to parylene-c, and commercialized it through the company Cyberkinetics. These efforts are the leading candidate for the first human trials on a broad scale for motor cortical implants to help quadriplegic or trapped patients communicate with the outside world.

[edit] Related reading

^{^} Lebedev, M.A., Carmena, J.M., O’Doherty, J.E., Zacksenhouse, M., Henriquez, C.S., Principe, J.C., Nicolelis, M.A.L. (2005), Cortical ensemble adaptation to represent actuators controlled by a brain-machine interface. J. Neurosci. 25: 4681-4693 [1]
Donoghue JP, "Connecting cortex to machines: recent advances in brain interfaces." Nat Neurosci., 2002 Nov;5 Suppl:1085-8.
Lebedev, M.A., Carmena, J.M., O’Doherty, J.E., Zacksenhouse, M., Henriquez, C.S., Principe, J.C., Nicolelis, M.A.L. (2005) Cortical ensemble adaptation to represent actuators controlled by a brain machine interface.
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