Neural Plasticity Research Paper

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Neural plasticity refers to the ability of neurons to change in form and function in response to alterations in their environment. Neurons function as parts of local circuits in the brain, and each neuron can change its functional role in a circuit by altering how it responds to inputs or influences other neurons. Neuronal interactions for computational functions largely depend on synaptic relationships, and neural plasticity largely results from changes in the strengths of synaptic connections between neurons and the formation of new connections. Neural plasticity occurs as neurons respond to the activities of neighboring neurons that are spontaneously active or are activated by events in the external environment, and to trophic and guidance factors released in the local environment. Neural plasticity is essential for the normal development of brain circuits, creating the differences in those circuits that make us individuals. Neural plasticity mediates the acquisition of knowledge and skill, and brain repair after injury. Plasticity may also lead to misperceptions and pain, and maladaptive behavior. An understanding of neural plasticity might help us promote this plasticity when it is useful, and control this plasticity when it has unfortunate consequences.

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1. Neural Plasticity During Brain Development

The basic circuitry of the brain gradually emerges during development. While the mature brain remains plastic, developmental changes are especially impressive. For example, a short period of sensory loss, such as produced by having an eye covered by a patch early in childhood, can have a devastating effect on vision for that eye. The brain circuits for vision become dominated by the seeing eye so that connections and synaptic strengths change, deprived neurons fail to grow and axon branches withdraw, and a deficit in vision for the closed eye occurs that persists after the eye patch is removed (Antonini and Stryker 1993). A similar period of deprivation in adults has little effect. The developing brain is especially plastic because it is using information from the environment to help construct itself (Rauschecker 1991, Schatz 1990). Slight changes in the instructions from the environment, and the timing of those instructions can lead to quite different outcomes. In the mature brain, the circuits have been built, and further modifications are usually less profound.

One of the important accomplishments of developmental plasticity is to create functionally adaptive circuits in the brain. Developmental plasticity refers to the capacity of the brain to have different developmental outcomes. The development of some brain circuits, some of those in simple invertebrates for example, may be highly fixed. Thus, the developing circuits usually achieve the same adult form. But, this is not necessarily the case for the complex circuits of the higher brain centers of mammals, especially those in humans with long periods of development. The human brain is highly plastic because the brain circuits are not fully specified by the genes. All of the necessary information for proper development does not reside in the genes or gene products. Thus, it is necessary to use information from the environment to direct development. Neurons are designed to respond to sensory stimuli and each other with action potentials or spikes. Self-generated spontaneous activity and evoked activity are very important in mediating normal development (Schatz 1990). Neurons also influence the development of other neurons through the release of trophic and guidance factors (Connor and Dragunow 1998).

Consistencies in the internal and external environments during development typically lead to the development of similar brains with very similar brain circuits. Because the developmental outcomes can be so similar, the role of the environment may not always be obvious. Thus, one way to study developmental plasticity is to rear animals in abnormal environments (Rauschecker 1991). As examples, the development of the visual system can be altered by rearing mammals in the dark, with one eye closed, or under strobe lights. These experiments indicate that sensitivity to the environment is an important component of the normal development of brain circuits. In an abnormal environment, development can be misdirected, often with unfortunate functional consequences.

Sensitivity to the environment also allows the developing nervous system to become tailored to specifics of the environment of the individual. The newly hatched bird imprints on its parents, rather than birds in general, although even a moving box or balloon will do in the absence of tending parents. The young bird can become completely attached to such obviously false parents. The child that practices piano or basketball becomes the great piano or basketball player. Humans learn the sounds of their own language, and as adults find it hard to process the sounds of other languages. Thus, neural plasticity allows the brain to adapt to an uncertain environment, and permits specializing the formation of neural circuits within individuals for individual needs.

Because neuronal circuits are designed to be altered by aspects of the environment at certain times in development, or later during critical points in the lifecycle, there are changes in circuits that are possible only at certain times, and these changes are often difficult or impossible to reverse. These times are called critical or sensitive periods. Eye patching for a period of days to weeks, for example, will greatly alter brain circuits, only during a fixed early period of visual development. Earlier or later periods of deprivation have little effect. There may be a critical or sensitive period for song birds learning songs, for human language to be easily and flawlessly acquired, and for learning perfect pitch.

In summary, neural plasticity is essential for normal brain development, especially for the development of large complex brains that mature slowly. The normal development of the human brain is especially dependent on neuronal plasticity. Many circuits require information from the environment to be designed properly. In addition, neuronal plasticity allows the development of the individual, and individual skills and abilities.

2. Neural Plasticity And The Lifecycle

Neural plasticity also allows brain circuits to function differently at different phases of the lifecycle. Hormones play a major role in adjusting neural circuits. Song birds, for example, adjust and even add new neurons to the neural circuits used in producing and acquiring songs used during the breeding season (Konishi 1985). At puberty, humans and other mammals alter brain circuits that mediate aspects of sexual behavior, and later brain circuits are adjusted to promote maternal and paternal behaviors. Thus, plasticity permits rapid and functionally important changes in brain circuits as life styles change with puberty and parenthood.

3. Neural Plasticity And Learning

Learning is based on neural plasticity. Each individual acquires a great deal of useful information about the environment through experience, and improves and perfects a great number of motor skills. The importance of learning varies with species, and it is probably most important in humans. There are several types of learning, but they all depend on modifying the functional circuits of neurons.

The neuronal mechanisms of learning are not fully understood, although they have been under intensive study for many years. It is likely that two types of induced changes in synaptic effectiveness between neurons are important in most learning. When a source of input to a neuron or group of neurons is intensely stimulated for a brief period of time, later stimulations might be more effective and produce a greater response. This change in synaptic effectiveness, which may persist for minutes to hours or longer, has been called long-term potentiation (LTP; see Bliss and Lomo 1973). Of course, new learning involves for-getting, so that connection strengths need to be weakened as well. Patterns of less intense, more distributed stimulation may reduce synaptic effectiveness. This reduction is called long-term depression (LTD; see Nelson and Turrigiano 1998). Possibly, LTP depends on reversing LTD.

Both LTP and LTD are likely to be critical components of memory formation and the acquisition of skills. LTP and LTD have been most studied in the hippocampus, both in a tissue slice preparation, which offers clear technical advantages, and in the intact animal. LTP and LTD are components of what has been called Hebbian plasticity (see Brown et al. 1988, Rauscheker 1991) after the neuropsychologist, Donald Hebb. In an effort to account for learning, Hebb theorized that the repeated activations of local neuron circuits changed the effectiveness of pathways so that some inputs came to activate the circuits more easily and more effectively. If neuron A takes part in the firing of neuron B, the future effectiveness of neuron A in firing neuron B is increased. The cellular mechanisms of Hebbian plasticity have been studied, and they involve the activation of the NMDA (N-methylD-aspartate) glutamate receptor and a calcium influx into the post synaptic neuron when pre synaptic activity is paired with post synaptic depolarization (Bear 1995, Rauschecker 1991). The hippocampus is known to have a critical early role in the formation of long-term memories, but it is not generally thought to be the site of permanent storage. The amygdala encodes the emotional component of memories formed during fear conditioning, but like the hippocampus, the neuronal plasticity that occurs in the amygdala may modulate the consolidation of memories formed elsewhere.

Most memories and skills depend on neocortex. LTP and LTD also have been demonstrated in neocortex circuits where these types of synaptic plasticity are likely to be important in the consolidation and storage of information.

4. Neural Plasticity And Brain Repair

Neural plasticity is also important in brain reorganization and repair after injury. The effects of sensory loss have been extensively studied in the sensory systems of adult mammals (Kaas 1991, Kaas et al. 1999). Sensory loss of one type or another commonly occurs during adult life. For example, humans typically lose auditory receptors and, especially, high-frequency hearing as they age. Studies in monkeys, cats, and rodents show that auditory cortex reorganizes after such partial hearing loss so that more neurons are devoted to processing the remaining inputs. The functional significance of this reorganization is not clear, but it may help individuals adjust to the hearing loss and more effectively use the remaining inputs. Similar changes occur when small portions of the retina are damaged. The regions of visual cortex that are deprived of their normal sources of activation by such damage soon come to be responsive to surrounding intact parts of the retina.

Finally, any restricted loss of tactile inputs from the skin, such as those caused by nerve damage, is followed by a reorganization of somatosensory cortex so that deprived neurons become responsive to preserved tactile afferents. Such findings indicate that the brains of even adult mammals have considerable capacity for functional reorganization so that neurons that are deprived of a normal source of activation gradually acquire new sources of activation. Unresponsive neurons are not of much use, and the reactivation of deprived neurons, as a common feature of brain damage, may greatly contribute to behavior recovery and compensation. The mature brain may well be designed to compensate for some neuronal loss and damage, and reorganization may lead to more effective use of remaining neurons and neural circuits.

Humans and other mammals compensate remarkably well from cortical damage that is relatively restricted. In part, this may be the result of reorganization within the damaged area of cortex. Sensory and motor representations in cortex reorganize after damage to recover some of the lost parts of the representation. Other intact areas of cortex may reorganize to help compensate for the loss. During some period of brain development, parts of the brain may be capable of regenerating lost neurons (Kolb et al. 1998).

Impressive recoveries after brain damage may reflect design features involving plasticity, or even the fortunate utilization of mechanisms built in by selection for normal development and adult learning. However, plasticity is not always beneficial. The plasticity that is there for one set of purposes may be evoked in other sets of circumstances where the results are detrimental and unfortunate. As one example, individuals with amputated limbs typically feel that the missing limb is still there (Ramachandran and Blakeslee 1998). This may be the result of neurons in the brain, deprived of normal sources of activation by afferents from the missing limb, becoming more sensitive to intrinsic signals or other inputs. The growth of new connections in the brain stem and cortex seems to add the further complexity of trigger zones, locations on the face and stump that, if touched, evoke a sensation in the missing limb. Fortunately, this type of misperception is not very disturbing. However, severe pain also might be felt in the missing limb, apparently as a result of the plasticity of circuits in the thalamus. This pain is very difficult to treat since it is not generated in the normal way.

As another example of maladaptive plasticity, individuals that overpractice a skill may develop motor disorders or dystonias (Byl et al. 1996). Neural plasticity is essential for developing motor skills, but musicians and writers may overpractice or overuse a skill so that performance deteriorates rather than improves. The practice may coactivate neurons so frequently that they become so strongly interconnected that they fail to respond independently when needed in other neuronal circuits. Thus, the musician loses control of the skilled hand movements needed to play, and the writer develops writer’s cramp. Recoveries depend on other training and experiences that rebalance the motor circuits.

5. Mechanisms Of Neural Plasticity

Brain circuits are plastic because new connections form, unused connections are lost, and existing connections increase or decrease in effectiveness. Developing brains are especially plastic because it is a time of great neuronal growth. Activity-dependent genes (Kaczmarek and Chaudhuri 1997) within neurons function to promote and direct new growth, or stop growth, and cause retractions of axons and dendrites and even cell death. The developing nervous system over-produces neurons and connections, and uses activity patterns induced in neurons by the external and internal environments to select the useful, more active neurons and connections and eliminate other less active neurons and connections. By altering activity patterns through lesions, drugs, and experience, outcomes can be changed so that normally lost neurons are saved, normally lost connections are preserved, and even new growth occurs. One of the early discoveries was that rats reared in a complex rather than a simple environment (Greenough et al. 1985) developed a thicker cortex with larger neurons and more complex dendritic arbors. As a more unusual, more dramatic, example of developmental plasticity, rodents reared after a major loss of auditory inputs to the forebrain grow visual inputs into the auditory thalamus, so that auditory cortex is activated by visual stimuli (Sur et al. 1988). The potential for the growth as well as the loss of new connections is great in the developing brain.

Neuronal growth and death can be a feature of normal lifestyle changes as well. Neurons may increase in size and connectional complexity in brain regions related to sexual behavior or bird song during appropriate parts of the breeding season, and then shrink and disconnect later (Konishi 1985). Neurons may even be born and added to such circuits, to later die. While neuronal growth and even death are major components of programmed plasticity for expected developmental and lifecycle events, much less new growth or retraction might be expected at other times in the mature brain, which has developed brain circuits for a period of stable performance. Indeed, except for learning and learning mechanisms, the mature brain has been considered to be rather fixed in organization and not plastic. Now, considerable evidence has accumulated to show that the functional organization of the mature brain is quite mutable, and that at least some of the changes depend on new growth. In cases of severe sensory loss, such as with brain or spinal cord lesions, or peripheral nerve damage, growth of axons over considerable distances occurs to reactivate deprived neurons in the spinal cord, brainstem, and cortex. While extensive new growth in the mature brain is often likely to be detrimental, and glial cells in the central nervous system produce factors that inhibit such new growth, the local growth of axons and dendrites is probably ongoing and common. In addition, the cellular factors for inhibiting more extensive growth may be overcome by extreme deprivation. It remains to be demonstrated how much new growth contributes to behavioral recoveries after brain damage, but a major contribution by new growth seems likely. In addition, new neurons appear to be added to neocortex and other parts of the forebrain throughout life (Gould et al. 1999, Van Praag et al. 1999). While neurogenesis had been thought to be limited to the period of brain development, recent evidence for the addition of neurons to the mature primate brain raises the possibility that such new neurons contribute to brain plasticity.

A common and possibly more powerful factor in neural plasticity is increasing or decreasing the effectiveness of existing connections. This can be done by increasing or decreasing the number, sizes, and positions of synapses, the amount of neurotransmitter released, and the receptor sites responsive to the transmitter. The important roles of LTP and LTD have already been discussed. These mechanisms may be potentiated by the appropriate release of neuromodulators that increase neural activity for short but behaviorally significant periods of time. Thus, stressful and other motivating events activate brainstem neurons that release the neurotransmitter, acetylcholine (ACh) throughout the brain where synaptic strengths are likely to be modified. This makes the changes in neural circuits more likely, so that the motivating events can be retained in memory and skills can be acquired more readily. The permissive effects of ACh release on neural plasticity can even be obtained artificially by electrically stimulating the brainstem neurons that project to cortex and release ACh during learning (Kilgard and Merzenich 1998).

There are many other ways of promoting neural plasticity. Neurons tend to self-regulate through the actions of activity-dependent genes to reach a set level of activity. Neurons with lowered levels of activity tend to express lower levels of the inhibitory neurotransmitter, GABA, or become less sensitive to GABA by making fewer GABA receptors (Hendry and Jones 1998). More active neurons make more GABA and more GABA receptors. Thus, deprived neurons become more sensitive and respond to inputs that were previously subthreshold and ineffective, while overactive neurons lose responsiveness to weak but previously effective inputs. Other activity-dependent genes probably regulate neuron growth through the release of trophic and guidance factors.

6. Conclusions

Neural plasticity is important for the normal development and maintenance of neural circuits. This plasticity adjusts mature brain circuits to mediate individual perceptual and motor skills, and adaptive adjustments to an uncertain environment. Neural plasticity is especially important in storing information. Plasticity also functions in brain repair. Because some outcomes of neuronal plasticity are highly desirable, while others are unfortunate, a comprehensive understanding of the mechanisms of plasticity and how to control them would be clinically and therapeutically beneficial.


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