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synaptic plasticity and non-synaptic plasticityit refers to changes in neural pathways and
synapses which are due to changes in behavior, environment and neural processes, as well as
changes resulting from bodily injury.[1] Neuroplasticity has replaced the formerly-held position
that the brain is a physiologically static organ, and explores how - and in which ways - the brain
changes throughout life.[2]
Neuroplasticity occurs on a variety of levels, ranging from cellular changes due to learning, to
large-scale changes involved in cortical remapping in response to injury. The role of
neuroplasticity is widely recognized in healthy development, learning, memory, and recovery
from brain damage. During most of the 20th century, the consensus among neuroscientists was
that brain structure is relatively immutable after a critical period during early childhood. This
belief has been challenged by findings revealing that many aspects of the brain remain plastic
even into adulthood.[3]
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.[4] 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.[5]
Decades of research[6] 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. Neuroscientific research indicates that experience can actually change
both the brain's physical structure (anatomy) and functional organization (physiology).
Neuroscientists are currently engaged in a reconciliation of critical period studies demonstrating
the immutability of the brain after development with the more recent research showing how the
brain can, and does, change.[7]
Contents
1 Neurobiology
o 1.1 Cortical maps
3 Etymology
4 History
o 4.1 Proposal
o 4.2 Research and discovery
5 See also
6 References
7 Further reading
8 External links
Neurobiology
One of the fundamental principles of how neuroplasticity functions is linked to the concept of
synaptic pruning, the idea that individual connections within the brain are constantly being
removed or recreated, largely dependent upon how they are used. This concept is captured in the
aphorism, "neurons that fire together, wire together"/"neurons that fire apart, wire apart." If there
are two nearby neurons that often produce an impulse simultaneously, their cortical maps may
become one. This idea also works in the opposite way, i.e. that neurons which do not regularly
produce simultaneous impulses will form different maps.
Cortical maps
Cortical organization, especially for the sensory systems, is often described in terms of maps.[8]
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, Jon Kaas and Doug Rasmusson used the
cortical map as their dependent variable. They foundand this has been since corroborated by a
wide range of labsthat if the cortical map is deprived of its input it will become activated at a
later time in response to other, usually adjacent inputs. Merzenichs (1984) study involved the
mapping of owl monkey hands before and after amputation of the third digit. Before amputation,
there were five distinct areas, one corresponding to each digit of the experimental hand. Sixtytwo days following amputation of the third digit, the area in the cortical map formerly occupied
by that digit had been invaded by the previously adjacent second and fourth digit zones. The
areas representing digit one and five are not located directly beside the area representing digit
three, so these regions remained, for the most part, unchanged following amputation.[9] This
study demonstrates that only those regions bordering a certain area will invade it to alter the
cortical map. 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.[10]
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 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 threefold in 12 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. Phantom
limbs are experienced by people that have undergone amputations in hands, arms, and legs, but it
is not limited to extremities. Although the neurological basis of phantom limbs is still not entirely
understood it is believed that cortical reorganization plays an important role.[11]
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". Changes such as 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 "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.[11][12]
A 2005 study found that the effects of neuroplasticity occur even more rapidly than previously
expected. Medical students' brains were imaged during the period when they were studying for
their exams. In a matter of months, the students' gray matter increased significantly in the
posterior and lateral parietal cortex.[13]
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.
Paul Bach-y-Rita, deceased in 2006, was the "father of sensory substitution and brain
plasticity."[14] In working with a patient whose vestibular system had been damaged he developed
BrainPort,[15] a machine that "replaces her vestibular apparatus and [will] send balance signals to
her brain from her tongue."[11] After she had used this machine for some time it was no longer
necessary, as she regained the ability to function normally. Her balancing act days were over.[16]
Plasticity is the major explanation for the phenomenon. Because her vestibular system was
"disorganized" and sending random rather than coherent signals, the apparatus found new
pathways around the damaged or blocked neural pathways, helping to reinforce the signals that
were sent by remaining healthy tissues. Bach-y-Rita explained plasticity by saying, "If you are
driving from here to Milwaukee and the main bridge goes out, first you are paralyzed. Then you
take old secondary roads through the farmland. Then you use these roads more; you find shorter
paths to use to get where you want to go, and you start to get there faster. These "secondary"
neural pathways are "unmasked" or exposed and strengthened as they are used. The "unmasking"
process is generally thought to be one of the principal ways in which the plastic brain reorganizes
itself."[11]
Randy Nudo's group found that if a small stroke (an infarction) is induced by obstruction of
blood flow to a portion of a monkeys motor cortex, the part of the body that responds by
movement will move when areas adjacent to the damaged brain area are stimulated. In one study,
intracortical microstimulation (ICMS) mapping techniques were used in nine normal monkeys.
Some underwent ischemic infarction procedures and the others, ICMS procedures. The monkeys
with ischemic infarctions retained more finger flexion during food retrieval and after several
months this deficit returned to preoperative levels.[17] With respect to the distal forelimb
representation, "postinfarction mapping procedures revealed that movement representations
underwent reorganization throughout the adjacent, undamaged cortex."[17] Understanding of
interaction between the damaged and undamaged areas provides a basis for better treatment
plans in stroke patients. Current research includes the tracking of changes that occur in the motor
areas of the cerebral cortex as a result of a stroke. Thus, events that occur in the reorganization
process of the brain can be ascertained. Nudo is also involved in studying the treatment plans
that may enhance recovery from strokes, such as physiotherapy, pharmacotherapy and electrical
stimulation therapy.
Neuroplasticity is gaining popularity as a theory that, at least in part, explains improvements in
functional outcomes with physical therapy post stroke. Rehabilitation techniques that have
evidence to suggest cortical reorganization as the mechanism of change include Constraintinduced movement therapy, functional electrical stimulation, treadmill training with body weight
support, and virtual reality therapy. Robot assisted therapy is an emerging technique, which is
also hypothesized to work by way of neuroplasticity, though there is currently insufficient
evidence to determine the exact mechanisms of change when using this method.[18]
Jon Kaas, a professor at Vanderbilt University, has been able to show "how somatosensory area
3b and ventroposterior (VP) nucleus of the thalamus are affected by long standing unilateral
dorsal column lesions at cervical levels in macaque monkeys."[19] Adult brains have the ability to
change as a result of injury but the extent of the reorganization depends on the extent of the
injury. His recent research focuses on the somatosensory system, which involves a sense of the
body and its movements using many senses. Usually when people damage the somatosensory
cortex, impairment of the body perceptions are experienced. He is trying to see how these
systems (somatosensory, cognitive, motor systems) are plastic as a result of injury.[19]
One of the most recent applications of neuroplasticity involves work done by a team of doctors
and researchers at Emory University, specifically Dr. Donald Stein (who has been in the field for
over three decades)[20] and Dr. David Wright. This is the first treatment in 40 years that has
significant results in treating traumatic brain injuries while also incurring no known side effects
and being cheap to administer.[21] Dr. Stein noticed that female mice seemed to recover from
brain injuries better than male mice. Also in females, he noticed that at certain points in the
estrus cycle females recovered even more. After lots of research, they attributed this difference
due to the levels of progesterone. The highest level of progesterone present led to the fastest
recovery of brain injury in these mice.
They developed a treatment that includes increased levels of progesterone injections to give to
brain injured patients. "Administration of progesterone after traumatic brain injury[22] (TBI) and
stroke reduces edema, inflammation, and neuronal cell death, and enhance spatial reference
memory and sensory motor recovery."[23] In their clinical trials, they had a group of severely
injured patients that after the three days of progesterone injections had a 60% reduction in
mortality.[21] Sam* was in a horrific car accident that left him with marginal brain activity;
according to the doctors, he was one point away from being brain dead. His parents decided to
have him participate in Dr. Steins clinical trial and he was given the three-day progesterone
treatment. Three years after the accident, he had achieved an inspiring recovery with no brain
complications and the ability to live a healthy, normal life.[21]
Stein has done some studies in which beneficial effects have been seen to be similar in aged rats
to those seen in youthful rats. As there are physiological differences in the two age groups, the
model was tweaked for the elderly animals by reducing their stress levels with increased physical
contact. During surgery, anesthesia was kept at a higher oxygen level with lower overall
isoflurane percentage and "the aged animals were given subcutaneous lactated ringers solution
post-surgery to replace fluids lost through increased bleeding."[24] The promising results of
progesterone treatments "could have a significant impact on the clinical management of TBI."[24]
These treatments have been shown to work on human patients who receive treatment soon after
the TBI. However, Dr. Stein now focuses his research on those persons who have longstanding
traumatic brain injury in order to determine if progesterone treatments will assist them in the
recovery of lost functions as well.
Vision
After decades in which the assumption that binocular vision, in particular stereopsis, had to be
achieved in early childhood lest it could never be gained, in recent years the successful
Sensory prostheses
Neuroplasticity is involved in the development of sensory function. The brain is born immature
and it adapts to sensory inputs after birth. In the auditory system, congenital hearing impairment,
a rather frequent inborn condition affecting 1 of 1000 newborns, has been shown to affect
auditory development, and implantation of a sensory prostheses activating the auditory system
has prevented the deficits and induced functional maturation of the auditory system [29] Due to a
sensitive period for plasticity, there is also a sensitive period for such intervention within the first
24 years of life. Consequently, in prelingually deaf children, early cochlear implantation as a
rule allows to learn mother language and acquire acoustic communication.[30]
Phantom limbs
A diagrammatic explanation of the mirror box. The patient places the good limb into one side of
the box (in this case the right hand) and the amputated limb into the other side. Due to the mirror,
the patient sees a reflection of the good hand where the missing limb would be (indicated in
lower contrast). The patient thus receives artificial visual feedback that the "resurrected" limb is
now moving when they move the good hand.
Main articles: Phantom limb and Mirror box
The experience of Phantom limbs is a phenomenon in which a person continues to feel pain or
sensation within a part of their body which has been amputated. This is strangely common,
occurring in 60-80% of amputees.[31] An explanation for this refers to the concept of
neuroplasticity, as the cortical maps of the removed limbs are believed to have become engaged
with the area around them in the postcentral gyrus. This results in activity within the surrounding
area of the cortex being misinterpreted by the area of the cortex formerly responsible for the
amputated limb.
The relationship between phantom limbs and neuroplasticity is a complex one. In the early 1990s
V.S. Ramachandran theorized that phantom limbs were the result of cortical remapping.
However, in 1995 Herta Flor and her colleagues demonstrated that cortical remapping occurs
only in patients who have phantom pain.[32] Her research showed that phantom limb pain (rather
than referred sensations) was the perceptual correlate of cortical reorganization.[33] This
phenomenon is sometimes referred to as maladaptive plasticity.
In 2009 Lorimer Moseley and Peter Brugger carried out a remarkable experiment in which they
encouraged arm amputee subjects to use visual imagery to contort their phantom limbs into
impossible configurations. Four of the seven subjects succeeded in performing impossible
movements of the phantom limb. This experiment suggests that the subjects had modified the
neural representation of their phantom limbs and generated the motor commands needed to
execute impossible movements in the absence of feedback from the body.[34] The authors stated
that:"In fact, this finding extends our understanding of the brain's plasticity because it is evidence
that profound changes in the mental representation of the body can be induced purely by internal
brain mechanisms--the brain truly does change itself."
Chronic Pain
Main article: Chronic pain
Individuals who suffer from chronic pain experience prolonged pain at sites that may have been
previously injured, yet are otherwise currently healthy. This phenomenon is related to
neuroplasticity due to a maladaptive reorganization of nervous system, both peripherally and
centrally. During the period of tissue damage, noxious stimuli and inflammation cause an
elevation of nociceptive input from the periphery to the central nervous system. Prolonged
nociception from periphery will then elicit a neuroplastic response at the cortical level to change
its somatotopic organization for the painful site, inducing central sensitization.[35] For instance,
individuals experiencing complex regional pain syndrome demonstrate a diminished cortical
somatotopic representation of the hand contralaterally as well as a decreased spacing between the
hand and the mouth.[36] Additionally, chronic pain has been reported to significantly reduce the
volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and
right thalamus.[37] However, following treatment, these abnormalities in cortical reorganization
and grey matter volume are resolved, as well as their symptoms. Similar results have been
reported for phantom limb pain,[38] chronic low back pain[39] and carpal tunnel syndrome.[40]
Meditation
Main article: Research on meditation
A number of studies have linked meditation practice to differences in cortical thickness or
density of gray matter. One of the most well-known studies to demonstrate this was led by Sara
Lazar, from Harvard University, in 2000.[41] Richard Davidson, a neuroscientist at the University
of Wisconsin, has led experiments in cooperation with the Dalai Lama on effects of meditation
on the brain. His results suggest that long-term, or short-term practice of meditation results in
different levels of activity in brain regions associated with such qualities as attention, anxiety,
depression, fear, anger, the ability of the body to heal itself, and so on. These functional changes
may be caused by changes in the physical structure of the brain.[42][43][44][45]
from it. Then, over the next four weeks they allowed one group of mice to run inside their rodent
wheels, an activity most mice enjoy, while they forced the other group to work harder on
minitreadmills at a speed and duration controlled by the scientists. They then tested both groups
again to track their learning skills and memory. Both groups of mice improved their
performances in the water maze from the earlier trial. But only the extra-worked treadmill
runners were better in the avoidance task, a skill that, according to neuroscientists, demands a
more complicated cognitive response.[46]
The mice who were forced to run on the treadmills showed evidence of molecular changes in
several portions of their brains when viewed under a microscope, while the voluntary wheelrunners had changes in only one area. "Our results support the notion that different forms of
exercise induce neuroplasticity changes in different brain regions," Chauying J. Jen, a professor
of physiology and an author of the study, said.[47]
Human echolocation
Human echolocation is a learned ability for humans to sense their environment from echoes. This
ability is used by some blind people to navigate their environment and sense their surroundings
in detail. Studies in 2010 [48] and 2011 [49] using Functional magnetic resonance imaging
techniques have shown that parts of the brain associated with visual processing are adapted for
the new skill of echolocation. Studies with blind patients, for example, suggest that the clickechoes heard by these patients were processed by brain regions devoted to vision rather than
audition.[50]
Neuroplasticity in Animals
See also: Brain development and Neural development in humans
In a single lifespan, individuals in an animal species may encounter various changes in brain
morphology. Many of these differences are caused by the release of hormones in the brain;
others are the product of evolutionary factors or developmental stages.[51] [52] [53] [54] Some changes
occur seasonally in species to enhance or generate response behaviors.
Seasonal brain changes
Changing brain behavior and morphology to suit other seasonal behaviors is relatively common
in animals.[55] These changes can improve the chances of mating during breeding season.[56][57][58]
[59][60] [61]
Examples of seasonal brain morphology change can be found within many classes and
species.
Within the class Aves, black-capped chickadees experience an increase in the volume of the
hippocampus and strength of neural connections to the hippocampus during fall months.[62][63]
This change in brain morphology for spatial memory within the hippocampus is not limited to
birds, and affects some rodents and amphibians.[64] In songbirds, many song control nuclei in the
brain increase in size during mating season.[65] Among birds, changes in brain morphology to
influence song patterns, frequency, and volume are common.[66] Gonadotropin-releasing hormone
Etymology
Plasticity was first applied to behavior in 1890 by William James in The Principles of
Psychology,[75] though the idea was largely neglected for the next fifty years[citation needed]. The first
person to use the term neural plasticity appears to have been the Polish neuroscientist Jerzy
Konorski.[76]
Given the central importance of neuroplasticity, an outsider would be forgiven for assuming that
it was well defined and that a basic and universal framework served to direct current and future
hypotheses and experimentation. Sadly, however, this is not the case. While many neuroscientists
use the word neuroplasticity as an umbrella term it means different things to different researchers
in different subfields ... In brief, a mutually agreed upon framework does not appear to exist.[77]
History
Proposal
Until around the 1970s, an accepted idea across neuroscience was that the nervous system was
essentially fixed throughout adulthood, both in terms of brain functions, as well as the idea that it
was impossible for new neurons to develop after birth.[78]
In 1793, Italian anatomist Michele Vicenzo Malacarne described experiments in which he paired
animals, trained one of the pair extensively for years, and then dissected both. He discovered that
the cerebellums of the trained animals were substantially larger. But, these findings were
eventually forgotten.[79] The idea that the brain and its functions are not fixed throughout
adulthood was proposed in 1890 by William James in The Principles of Psychology, though the
idea was largely neglected.[75]
In 1923, Karl Lashley conducted experiments on rhesus monkeys which demonstrated changes
in neuronal pathways, which he concluded to be evidence of plasticity, although despite this, as
well as further examples of research suggesting this, the idea of neuroplasticity was not widely
accepted by neuroscientists. However, more significant evidence began to be produced in the
1960s and after, notably from scientists including Paul Bach-y-Rita, Michael Merzenich along
with Jon Kaas, as well as several others.[78][80]
In the 1960s, Paul Bach-y-Rita invented a device that allowed blind people to read, perceive
shadows, and distinguish between close and distant objects. This "machine was one of the first
and boldest applications of neuroplasticity."[11] The patient sat in an electrically stimulated chair
that had a large camera behind it which scanned the area, sending electrical signals of the image
to four hundred vibrating stimulators on the chair against the patients skin. The six subjects of
the experiment were eventually able to recognize a picture of the supermodel Twiggy.[11]
It must be emphasized that these people were congenitally blind and had previously not been
able to see. Bach-y-Rita believed in sensory substitution; if one sense is damaged, your other
senses can sometimes take over. He thought the skin and its touch receptors could act as a retina
(using one sense for another[81]). In order for the brain to interpret tactile information and convert
it into visual information, it has to learn something new and adapt to the new signals. The brain's
capacity to adapt implied that it possessed plasticity. He thought, "We see with our brains, not
with our eyes."[11]
A tragic stroke that left his father paralyzed inspired Bach-y-Rita to study brain rehabilitation.
His brother, a physician, worked tirelessly to develop therapeutic measures which were so
successful that the father recovered complete functionality by age 68 and was able to live a
normal, active life which even included mountain climbing. "His fathers story was firsthand
evidence that a late recovery could occur even with a massive lesion in an elderly person."[11]
He found more evidence of this possible brain reorganization with Shepherd Ivory Franz's work.
[82]
One study involved stroke patients who were able to recover through the use of brain
stimulating exercises after having been paralyzed for years. "Franz understood the importance of
interesting, motivating rehabilitation: Under conditions of interest, such as that of competition,
the resulting movement may be much more efficiently carried out than in the dull, routine
training in the laboratory(Franz, 1921, pg.93)."[83] This notion has led to motivational
rehabilitation programs that are used today.
Michael Merzenich is a neuroscientist who has been one of the pioneers of neuroplasticity for
over three decades. He has made some of "the most ambitious claims for the field - that brain
exercises may be as useful as drugs to treat diseases as severe as schizophrenia - that plasticity
exists from cradle to the grave, and that radical improvements in cognitive functioning - how we
learn, think, perceive, and remember are possible even in the elderly."[11] Merzenichs work was
affected by a crucial discovery made by David Hubel and Torsten Wiesel in their work with
kittens. The experiment involved sewing one eye shut and recording the cortical brain maps.
Hubel and Wiesel saw that the portion of the kittens brain associated with the shut eye was not
idle, as expected. Instead, it processed visual information from the open eye. It was" as though
the brain didnt want to waste any cortical real estate and had found a way to rewire itself."[11]
This implied neuroplasticity during the critical period. However, Merzenich argued that
neuroplasticity could occur beyond the critical period. His first encounter with adult plasticity
came when he was engaged in a postdoctoral study with Clinton Woosley. The experiment was
based on observation of what occurred in the brain when one peripheral nerve was cut and
subsequently regenerated. The two scientists micromapped the hand maps of monkey brains
before and after cutting a peripheral nerve and sewing the ends together. Afterwards, the hand
map in the brain that was expected to be jumbled was nearly normal. This was a substantial
breakthrough. Merzenich asserted that "if the brain map could normalize its structure in response
to abnormal input, the prevailing view that we are born with a hardwired system had to be
wrong. The brain had to be plastic."[11]
per neuron (Gopnick, et al., 1999). This amount is about twice that of the average adult brain. As
we age, old connections are deleted through a process called synaptic pruning.
Synaptic pruning eliminates weaker synaptic contacts while stronger connections are kept and
strengthened. Experience determines which connections will be strengthened and which will be
pruned; connections that have been activated most frequently are preserved. Neurons must have
a purpose to survive. Without a purpose, neurons die through a process called apoptosis in which
neurons that do not receive or transmit information become damaged and die. Ineffective or
weak connections are "pruned" in much the same way a gardener would prune a tree or bush,
giving the plant the desired shape. It is plasticity that enables the process of developing and
pruning connections, allowing the brain to adapt itself to its environment.
been widely studied in humans, data indicate that similar (though less effective) changes occur in
human brains following injury.
suffered massive strokes were able to regain functioning, demonstrating that the brain was much
more malleable than previously believed. Modern researchers have also found evidence that the
brain is able to rewire itself following damage.
2. It involves a variety of processes; plasticity is ongoing throughout life and involves brain
cells other than neurons, including glial and vascular cells.
3. It can happen for two different reasons; as a result of learning, experience and memory
formation, or as a result of damage to the brain.
4. Environment plays an essential role in the process, but genetics can also have an
influence.
The first few years of a child's life are a time of rapid brain growth. At birth, every neuron in the
cerebral cortex has an estimated 2,500 synapses; by age of three, this number has grown to a
whopping 15,000 synapses per neuron.
The average adult, however, has about half that number of synapses. Why? Because as we gain
new experiences, some connections are strengthened while others are eliminated. This process is
known as synaptic pruning. Neurons that are used frequently develop stronger connections and
those that are rarely or never used eventually die. By developing new connections and pruning
away weak ones, the brain is able to adapt to the changing environment.
Functional Plasticity: Refers to the brain's ability to move functions from a damaged area
of the brain to other undamaged areas.
Structural Plasticity: Refers to the brain's ability to actually change its physical structure
as a result of learning.
There are three different types of brain plasticity. The first occurs when infants are born and start
developing into children. Studies have shown that the immature brain grows and creates neural
networks at an unprecedented rate, as the brain is flooded with new sensory input from the
outside world. The second type occurs over the course of a lifetime, as the brain changes with
age to reflect new experiences and events. Additionally, the brain demonstrates tremendous
plasticity in the wake of injury.
Ad
Without this characteristic, the brain would remain static, frozen at a particular point in time. It
allows the brain to do everything from learn how to speak to refining physical movements such
as those associated with playing a musical instrument. Every time the brain encounters
information, it reworks itself to accommodate it, and creates a map of the information it contains
so that it can readily retrieve information when it is needed. People always need to be able to
store and interpret new information, making brain plasticity critical to function at all ages.
In addition to reworking itself to store information and organize it effectively, the brain can also
repair itself, to some extent. When an area of the brain is damaged, the activities associated with
that region will sometimes move to another area of the brain, allowing the person to recover
functionality. This type of brain plasticity is critical for people recovering from brain injuries and
neurological disorders, as the damage may be permanent, but it can be possible to mitigate the
effects.
Numerous studies have been conducted on brain plasticity to explore the changes in cellular
structure which occur in the brain over time. A number of factors appear to contribute, from
hormones generated inside the body to environmental cues, and people appear to be able to
enhance the flexibility of the brain by exercising it, much like function of the musculoskeletal
system can be improved or modified with exercise.