Neuroplasticity

BIOLOGY
WRITTEN BY:
 Michael Rugnetta
See Article History

Alternative Title: neural plasticity

Neuroplasticity, 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. Although neural
networks also exhibit modularity and carry out specific functions, they retain
the capacity to deviate from their usual functions and to reorganize
themselves. In fact, for many years, it was considered dogma in the
neurosciences that certain functions were hard-wired in specific, localized
regions of the brain and that any incidents of brain change or recovery were
mere exceptions to the rule. However, since the 1970s and ’80s,
neuroplasticity has gained wide acceptance throughout the
scientific community as a complex, multifaceted, fundamental property of
the brain. (For more information about the anatomy and functions of the
brain and nervous system, see the article human nervous system.)

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Neurons (red), which are supported by glial cells such as astrocytes (green), retain the ability to
deviate from their usual functions and to reorganize themselves in response to new information. Institute
for Stem Cell Research/Getty Images

Rapid change or reorganization of the brain’s cellular or neural networks

can take place in many different forms and under many different
circumstances. Developmental plasticity occurs when neurons in the young
brain rapidly sprout branches and form synapses. Then, as the brain begins
to process sensory information, some of these synapses strengthen and
others weaken. Eventually, some unused synapses are eliminated
completely, a process known as synaptic pruning, which leaves behind
efficient networks of neural connections. Other forms of neuroplasticity
operate by much the same mechanism but under different circumstances
and sometimes only to a limited extent. These circumstances include
changes in the body, such as the loss of a limb or sense organ, that
subsequently alter the balance of sensory activity received by the brain. In
addition, neuroplasticity is employed by the brain during the reinforcement
of sensory information through experience, such as
in learning and memory, and following actual physical damage to the brain
(e.g., caused by stroke), when the brain attempts to compensate for lost
activity.

plasticity; Mozart effectNeuroscientist Richard Haier discusses plasticity and debunks the Mozart
effect, the notion that human intelligence can be improved by listening to classical music, especially
works by Wolfgang Amadeus Mozart.© World Science Festival

Today it is apparent that the same brain mechanisms—adjustments in the

strength or the number of synapses between neurons—operate in all these
situations. Sometimes this happens naturally, which can result in positive or
negative reorganization, but other times behavioral techniques or brain-
machine interfaces can be used to harness the power of neuroplasticity for
therapeutic purposes. In some cases, such as stroke recovery, natural adult
neurogenesis can also play a role. As a result, neurogenesis has spurred
an interest in stem cell research, which could lead to an enhancement of
neurogenesis in adults who suffer from stroke, Alzheimer
disease, Parkinson disease, or depression.

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Types Of Cortical Neuroplasticity
Developmental plasticity occurs most profoundly in the first few years of life
as neurons grow very rapidly and send out multiple branches, ultimately
forming too many connections. In fact, at birth, each neuron in
the cerebral cortex (the highly convoluted outer layer of the cerebrum) has
about 2,500 synapses. By the time an infant is two or three years old, the
number of synapses is approximately 15,000 per neuron. This amount is
about twice that of the average adult brain. The connections that are not
reinforced by sensory stimulation eventually weaken, and the connections
that are reinforced become stronger. Eventually, efficient pathways of
neural connections are carved out. Throughout the life of a human or other
mammal, these neural connections are fine-tuned through the organism’s
interaction with its surroundings. During early childhood, which is known as
a critical period of development, the nervous system must receive certain
sensory inputs in order to develop properly. Once such a critical period
ends, there is a precipitous drop in the number of connections that are
maintained, and the ones that do remain are the ones that have been
strengthened by the appropriate sensory experiences. This massive
“pruning back” of excess synapses often occurs during adolescence.

Lateral view of the right cerebral hemisphere of the human brain, shown in situ within the skull. A
number of convolutions (called gyri) and fissures (called sulci) in the surface define four lobes—the
parietal, frontal, temporal, and occipital—that contain major functional areas of the brain. Encyclopædia
Britannica, Inc.

American neuroscientist Jordan Grafman has identified four other types of

neuroplasticity, known as homologous area adaptation, compensatory
masquerade, cross-modal reassignment, and map expansion.

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Functional areas of the human brain.Encyclopædia Britannica, Inc.

Homologous area adaptation

Homologous area adaptation occurs during the early critical period of
development. If a particular brain module becomes damaged in early life, its
normal operations have the ability to shift to brain areas that do not include
the affected module. The function is often shifted to a module in the
matching, or homologous, area of the opposite brain hemisphere. The
downside to this form of neuroplasticity is that it may come at costs to
functions that are normally stored in the module but now have to make
room for the new functions. An example of this is when the right parietal
lobe (the parietal lobe forms the middle region of the cerebral hemispheres)
becomes damaged early in life and the left parietal lobe takes over
visuospatial functions at the cost of impaired arithmetical functions, which
the left parietal lobe usually carries out exclusively. Timing is also a factor in
this process, since a child learns how to navigate physical space before he
or she learns arithmetic.
Compensatory masquerade
The second type of neuroplasticity, compensatory masquerade, can simply
be described as the brain figuring out an alternative strategy for carrying out
a task when the initial strategy cannot be followed due to impairment. One
example is when a person attempts to navigate from one location to
another. Most people, to a greater or lesser extent, have an intuitive sense
of direction and distance that they employ for navigation. However, a
person who suffers some form of brain trauma and impaired spatial sense
will resort to another strategy for spatial navigation, such as memorizing
landmarks. The only change that occurs in the brain is a reorganization of
preexisting neuronal networks.
Cross-modal reassignment

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The third form of neuroplasticity, cross-modal reassignment, entails the
introduction of new inputs into a brain area deprived of its main inputs. A
classic example of this is the ability of an adult who has been blind since
birth to have touch, or somatosensory, input redirected to the visual cortex
in the occipital lobe (region of the cerebrum located at the back of the head)
of the brain—specifically, in an area known as V1. Sighted people,
however, do not display any V1 activity when presented with similar touch-
oriented experiments. This occurs because neurons communicate with one
another in the same abstract “language” of electrochemical impulses
regardless of sensory modality. Moreover, all the sensory cortices of the
brain—visual, auditory, olfactory (smell), gustatory (taste), and
somatosensory—have a similar six-layer processing structure. Because of
this, the visual cortices of blind people can still carry out
the cognitive functions of creating representations of the physical world but
base these representations on input from another sense—namely, touch.
This is not, however, simply an instance of one area of the brain
compensating for a lack of vision. It is a change in the actual functional
assignment of a local brain region.
Map expansion
Map expansion, the fourth type of neuroplasticity, entails the flexibility of
local brain regions that are dedicated to performing one type of function or
storing a particular form of information. The arrangement of these local
regions in the cerebral cortex is referred to as a “map.” When one function
is carried out frequently enough through repeated behaviour or stimulus,
the region of the cortical map dedicated to this function grows and shrinks
as an individual “exercises” this function. This phenomenon usually takes
place during the learning and practicing of a skill such as playing a musical
instrument. Specifically, the region grows as the individual
gains implicit familiarity with the skill and then shrinks to baseline once the
learning becomes explicit. (Implicit learning is the passive acquisition of
knowledge through exposure to information, whereas explicit learning is the
active acquisition of knowledge gained by consciously seeking out
information.) But as one continues to develop the skill over repeated
practice, the region retains the initial enlargement.
Map expansion neuroplasticity has also been observed in association with
pain in the phenomenon of phantom limb syndrome. The relationship
between cortical reorganization and phantom limb pain was discovered in
the 1990s in arm amputees. Later studies indicated that in amputees who
experience phantom limb pain, the mouth brain map shifts to take over
the adjacentarea of the arm and hand brain maps. In some patients, the
cortical changes could be reversed with peripheral anesthesia.

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Brain-Computer Interface
Some of the earliest applied research in neuroplasticity was carried out in
the 1960s, when scientists attempted to develop machines that interface
with the brain in order to help blind people. In 1969 American
neurobiologist Paul Bach-y-Rita and several of his colleagues published a
short article titled Vision substitution by tactile image projection, which
detailed the workings of such a machine. The machine consisted of a metal
plate with 400 vibrating stimulators. The plate was attached to the back of a
chair so that the sensors could touch the skin of the patient’s back. A
camera was placed in front of the patient and connected to the vibrators.
The camera acquired images of the room and translated them into patterns
of vibration, which represented the physical space of the room and the
objects within it. After patients gained some familiarity with the device, their
brains were able to construct mental representations of physical spaces
and physical objects. Thus, instead of visible light stimulating
their retinas and creating a mental representation of the world, vibrating
stimulators triggered the skin of their backs to create a representation in
their visual cortices. A similar device exists today, only the camera fits
inside a pair of glasses and the sensory surface fits on the tongue. The
brain can do this because it “speaks” in the same neural “language” of
electrochemical signals regardless of what kinds of environmental stimuli
are interacting with the body’s sense organs.

brain-computer interfaceFrom devices that enable monkeys to control robotic arms with their minds
to neural interfaces that could increase quality of life for the physically impaired, brain-computer
interface technologies have advanced significantly since the 1960s, when the first machines capable
of interfacing with the brain were developed.Science in Seconds (www.scienceinseconds.com)

Today neuroscientists are developing machines that bypass external sense

organs and actually interface directly with the brain. For example,
researchers implanted a device that monitored neuronal activity in the brain

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 of a female macaque monkey. The monkey used a joystick to move a
cursor around a screen, and the computer monitored and compared the
movement of the cursor with the activity in the monkey’s brain. Once the
computer had effectively correlated the monkey’s brain signals for speed
and direction to the actual movement of the cursor, the computer was able
to translate these movement signals from the monkey’s brain to the
movement of a robot arm in another room. Thus, the monkey became
capable of moving a robot arm with its thoughts. However, the major finding
of this experiment was that as the monkey learned to move the cursor with
its thoughts, the signals in the monkey’s motor cortex (the area of the
cerebral cortex implicated in the control of muscle movements) became
less representative of the movements of the monkey’s actual limbs and
more representative of the movements of the cursor. This means that the
motor cortex does not control the details of limb movement directly but
instead controls the abstract parameters of movement, regardless of the
connected apparatus that is actually moving. This has also been observed
in humans whose motor cortices can easily be manipulated into
incorporating a tool or prosthetic limb into the brain’s body image through
both somatosensory and visual stimuli.
For humans, however, less-invasive forms of brain-computer interfaces are
more conducive to clinical application. For example, researchers have
demonstrated that real-time visual feedback from functional magnetic
resonance imaging (fMRI) can enable patients to retrain their brains and
therefore improve brain functioning. Patients with emotional disorders have
been trained to self-regulate a region of the brain known as
the amygdala (located deep within the cerebral hemispheres and believed
to influence motivational behaviour) by self-inducing sadness and
monitoring the activity of the amygdala on a real-time fMRI readout. Stroke
victims have been able to reacquire lost functions through self-induced
mental practice and mental imagery. This kind of therapy takes advantage
of neuroplasticity in order to reactivate damaged areas of the brain or to
deactivate overactive areas of the brain. Today researchers are
investigating the efficacy of these forms of therapy for individuals who suffer
not only from stroke and emotional disorders but also from chronic pain,
psychopathy, and social phobia.
Michael Rugnetta

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