Neuroplasticity

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Overview

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Neuroplasticity challenges the idea that brain functions are fixed in certain locations.

Neuroplasticity (variously referred to as brain plasticity or cortical plasticity) refers to the changes that occur in the organization of the brain as a result of experience. A surprising consequence of neuroplasticity is that the brain activity associated with a given function can move to a different location as a consequence of normal experience or brain damage/recovery.

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.[1] 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[2]. Critical periods also were studied for language and suggested it was likely that the sensory pathways were fixed after their respective critical periods. Environmental changes could cause changes in behavior and cognition by modifying the connections of the new neurons in the hippocampus.

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 the brain's functional anatomy from top to bottom, if not also its physical anatomy. A proper reconciliation of critical period studies, which demonstrate some functional and anatomical aspects of neocortex are largely immutable after development, with the new findings on neuroplasticity, which demonstrate some functional aspects are highly mutable, are an active area of current research.

Canadian psychiatrist Norman Doidge has called neuroplasticity "one of the most extraordinary discoveries of the twentieth century."[3]

Brain plasticity and cortical maps

Cortical organization, especially for the sensory systems, is often described in terms of maps.[4] 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).

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 occurs at every level in the processing hierarchy to result in the map changes observed in the cerebral cortex.[5] It is not cortically emergent.

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 (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 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 thoughtTemplate:Specify 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.

The concept of plasticity can be applied to molecular as well as to environmental events.[citation needed] 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[attribution needed] 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.

Treatment of brain damage

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 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.[6] 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 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.

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. In these single day experiments, monkeys initially moved the actuator by pushing a joystick. After mapping out the motor neuron ensembles, control of the actuator was switched to the model of the ensembles so that the brain activity, and not the hand, directly controlled 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, within tens of minutes, 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.

Thought and neuroplasticity

The Dalai Lama invited Richard Davidson, a Harvard-trained neuroscientist at the University of Wisconsin-Madison's W.M. Keck Laboratory for Functional Brain Imaging and Behavior to his home in Dharamsala, India, in 1992 after learning about Davidson's innovative research into the neuroscience of emotions. Could the simple act of thinking change the mind? Most scientists believed this idea to be false, but they agreed to test the theory. One such experiment involved a group of eight Buddhist monk adepts and ten volunteers who had been trained in meditation for one week in Davidson's lab. All the people tested were told to meditate on compassion and love. Two of the controls, and all of the monks, experienced an increase in the number of gamma waves in their brain during meditation. As soon as they stopped meditating, the volunteers' gamma wave production returned to normal, while the monks, who had meditated on compassion for more than 10,000 hours in order to attain the rank of adept, did not experience a decrease to normal in the gamma wave production after they stopped meditating. The synchronized gamma wave area of the monks' brains during meditation on love and compassion was found to be larger than that corresponding activation of the volunteers' brains. Davidson's results were published in the Proceedings of the National Academy of Sciences in November, 1994 and TIME recognized Davidson as one of the ten most influential people in 2006 on the basis of his research.[7][8]

See also

Notes

  1. "Neurogenesis in adult primate neocortex: an evaluation of the evidence" Nature Reviews Neuroscience 3, 65-71 January 2002
  2. "The period of susceptibility to the physiological effects of unilateral eye closure in kittens"J Physiol Vol 206 1970, Issue 2 pp 419-436
  3. Doidge, Norman. The Brain that Changes Itself. Viking, 2007, p. xv.
  4. CORTICAL PLASTICITY: From Synapses to Maps DV Buonomano, MM Merzenich - Annual Review of Neuroscience, 1998
  5. Wall JT, Xu J, Wang X. "Human brain plasticity: an emerging view of the multiple substrates and mechanisms that cause cortical changes and related sensory dysfunctions after injuries of sensory inputs from the body." Brain Res Brain Res Rev. 2002 Sep;39(2-3):181-215.
  6. "Neurogenesis in adult primate neocortex: an evaluation of the evidence" Nature Reviews Neuroscience 3, 65-71 January 2002
  7. Lutz, A.; Greischar, L. L.; Rawlings, N. B.; Ricard, M.; Davidson, R. J. (2004-11-16), "Long-term meditators self-induce high-amplitude gamma synchrony during mental practice", PNAS, 101 (46): 16369–73, retrieved 2007-07-08
  8. The Dalai Lama. “How Thinking Can Change the Brain".

Further reading

de:Kortikale_Plastizität nl:Neurale plasticiteit


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