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Borrowing from Peter to Pay Paul ... Functional Plasticity Demonstrated in the Auditory Neocortex
In some situations
individuals can be born deaf, and one area of the brain normally reserved
for hearing appears to become a center for the processing of sign language.
These results were published by neuroscientists from Osaka
University Medical School in Japan in the January 14th issue
of the journal Nature Medicine.
These results further illustrate the extraordinary plasticity (flexibility)
of the developing brain.
For about 15
years now neuroscientists have know that sensory projection areas of the
neocortex are not arranged statically. That is to say, researchers
have known that certain regions of the neocortex have a propensity to process
certain sensory information, but the organization of these areas is not
exactly the same in every indivudual (or animal) (Module
5; Principles of Psychobiology). Moreover, when
the normal sensory input to the neocortex is altered in adult
anaimals, the spatial distribution of information processing in the neocortex
changes dramatically.
Researchers also
know that the developing brain can alter the "normal" spatial
organization of information processing. For example, previous studies have
found that blind subjects use areas of the brain's visual cortex to process
touch sensations related to the reading of Braille. Touch sensations
are normally sent to the somatosensory neocortex, located in the parietal
lobe.
Researchs from
Osaka University wondered if a similar 'borrowing' of neural space might
occur among the deaf as well. To evaluate this question they obtained positron
emission tomography (PET) scans of the brain of one individual born profoundly
deaf. The subject was instructed to watch sign-language videos during the
scanning procedure. The researchers point out that, among deaf subjects
with some experience with hearing, sign language (a visual medium) ''activates
the visual areas'' of the brain (occipital lobe).
However, PET
scans obtained from the congenitally deaf subject (preferentially) ``showed
activation of the auditory area in the sign-language task," within the
temporal neocortex. The fact that the subject used these regions for a
primarily visual language function provides ``striking evidence of neural
plasticity,'' the investigators conclude.
The subject under
study was scheduled to be fitted with a cochlear implant -- a device that
allows some profoundly deaf patients to detect certain sounds. The researchers
wondered if this individual's auditory areas might still be capable of
processing aural data.
An interesting
observation from the study relates to the primary auditory
neocortex, and the secondary auditory neocortex. According
to the authors, post-implantation PET scans indicated ``that (the) primary
auditory cortex still functions as an auditory area in this patient.''
They now believe that ``the primary auditory cortex of deaf people is reserved
for hearing sounds, whereas the secondary areas are used for processing
sign language.''
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A Receptor for Addiction?
A new receptor that has been identified by Dr. Catherine Ledant of the
Universit
libre de Bruxelles in Brussels, Belgium, may control responses
to both marijuana and heroin. Their findings are published in the January
15th issue of the journal
Science.
Drugs aimed at "switching off" the receptor might "be considered for preventing
the development of dependence on opiates and possibly other addictive drugs".
The authors findings show that chemicals found in marijuana bind to the
receptor CB1, and this type of receptor ``is abundant in the (cells of)
central and peripheral nervous systems.'' To determine the
role this receptor might play in marijuana dependence, the researchers
genetically engineered a line of 'knockout' mice born without functioning
CB1. A "knockout" mouse is a mouse that has been genetically altered so
that certain genes are missing that produce specific proteins, such as
those that comprise receptors.
In their study normal mice quickly began to display intoxication and addictive
behaviors after exposure to THC, the principle psychoactive compound found
in marijuana. However, the knockout mice who lacked functioning CB1 receptors
seemed unaffected by, and disinterested in, administration of THC. The
authors concluded that: "These results demonstrate that the main pharmacological
responses to (THC), as well as the addictive properties of cannabinoids,
are indeed mediated mostly, if not exclusively, by the CB1 receptor''.
In a second experiment, the investigators exposed knockout mice to morphine,
one of the opiate family of drugs that includes heroin. Both normal and
knockout mice showed typical intoxication to morphine. However, mice without
CB1 receptors seemed much less eager to self-administer the drug (via lever-pressing
with their nose), as compared to normal mice. According to the authors,
this suggests "that CB1 receptors are required for the development of physical
dependence'' on opiates.
If the results of the mouse study are duplicated in human trials, the CB1
receptor could present researchers with a 'two-in-one' target for new anti-addiction
drug therapies, Ledant's team speculates.
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What Can Amnesia Tell Us About Human Memory?
Although our memory system works reasonably well most of the time, sometimes things can go wrong. From a biological standpoint, information derived from brain pathology can give us clues as to how the normal human memory system works. The first feature in this section is a presentation by MSNBC news that describes amnesia, and contains illustrations about the human memory system.
WARNING:
Link to MSNBC's Amnesia Web Page
The second feature is an NPR interview that first describes an amnesic syndrome experienced by Mr. Terry Dibert. The interview with Dr. John Gabrieli at Stanford University also describes the case of H.M (Module 5: Principles of Psychobiology), and other amnesic effects.
More
on amnesia from National Public Radio...
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The Amygdala And Fear
The amygdala is recognized as a forebrain structure that controls fear and emotional responses an many species (Module 5: Principles of Psychobiology). The biological substrate of these processes relates that the type of connections established with the amygdala. For instance; the amygdala has many bidirectional connections with subcortical structures, as well as the frontal neocortical lobe, which also is recognized as a brain area that mediates emotions. Thus, the amygdala can be viewed as one central neural component of complex emotional response system. National Public Radio conducted an interview about the amygdala's role in emotional functions.
More
on the amygdala from National Public Radio...
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A 1995 audio interview with investigators who evaluated the neural substrares of emotional and factual memory. Convergent evidence from any sources indicates that the amygdala is involved in the processing of emotions.
More
on the amygdala and fear learning from National Public Radio...
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Is it Time Yet?
We have a fairly good ability to tell time; Not exactly like the clock
in your computer, but it works. Our ability to tell time is involved
in many of our behaviors, such as estimating when we should do something,
how
long we have been doing something, or when we should stop
doing
something once we have started it. Our ability to tell time also
is related to sleep and circadian cycles, because alterations in the sleep
cycle or circadian cycle (produced experimentally) will disrupt our
ability to estimate time. So, it seems that there might be a biological
clock somewhere in the brain that sets a time standard.
For many years, investigators have implicated certain areas of the brain
in this function, specifically small regions of the hypothalamus.
However, it has been unclear whether or not cells in the hypothalamus have
"endogenous" timers that are "built in", or whether they mearly respond
to input from millions of other brain cells.
Now, researchers have identified a specific population of cells in the
hypothalamus that serve as "pacemakers" for putative timing functions,
and they have shown that endogenous process in this subset of cells performs
the timing functions.
More
on "timing cells" from the BBC...
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Here For BBC© Link (REAL AUDIO (tm) INTERVIEW) (VIDEO)
NOTE: you will need
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RealPlayer for this interview.
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The Strength of Memories
We all know that some memories are established more easily than others.
And, most of us remember events that occur during highly emotional states.
Remember your first kiss? Remember your first date?
Previous research has shown that memories are affected by the body's chemical
response to emotional arousal: The body releases adrenaline and other hormones
into the blood, and it is widely recognized that high levels of arousal
can serve as a memory modulator. But for the most part, chemicals
that are produced in the body during highly emotional states, such as hormones,
can't cross the blood-brain barrier. So a major question has been: "How
does emotional state modulate memory?" A new study points
to the vagus nerve (N.X) (Module 5: Principles
of Psychobiology), which has two-way connections between the brainstem
and most of the body's internal organs. Results of this study may
help explain why emotionally charged events like falling in love, being
insulted, and family deaths evoke vivid memories, while everyday
recollections -- like where you ate lunch last week -- don't.
The results were published in the January issue of the journal Nature
Neuroscience by Robert Jensen and colleagues of Southern
Illinois University in Carbondale. The researchers evaluated
memory recall in 10 people involved in a medical study that tested whether
or not an implanted device that stimulates the vagus nerve could suppress
epileptic seizures. The device was approved for that use by federal regulators
last year.
Participants were tested before and after they got the nerve stimulators
implanted. During each session, they read a series of paragraphs that included
a total of 42 words highlighted with a yellow marker. In tests after implantation,
the vagus nerve was stimulated soon after they read individual paragraphs.
A short time later, they were tested on whether they could recognize the
target words in a list of about 250 words. They scored about 36 percent
better on recognizing words they'd read just before nerve stimulation,
compared with their performance before getting the implant.
Since the stimulation came after the words were read, it indicates that
the vagal nerve stimulation helps the brain store the memory of something
that just happened, rather than alerting the brain to pay attention to
what's coming up. The study also included sham stimulation procedures,
which showed that the memory boost after real stimulation wasn't just a
psychological effect of thinking the nerve had been activated.
"This is exciting new information that provides an important piece of the
puzzle" of how the hormones affect memory, said James McGaugh, director
of the Center for the Neurobiology of Learning and Memory at the University
of California, Irvine.
The vagus nerve is
kind of a two-way street. It relays orders from the brain to regulate things
like heart rate, while keeping the brain informed about what's going on
in the organs, such as whether the stomach is full.
McGaugh said emotional arousal affects memory routinely, not just during
extremely emotional events. Day to day, it's a way to help the brain separate
the wheat from the chaff of life: If something important has just happened,
the body gets aroused enough to cue the brain to remember it, he said.
Jensen doubts that nerve stimulation could help people with existing memory
impairments, such as patients with Alzheimer's disease, because memory
modulators work mostly to enhance memories, rather than produce
memories.
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The Role of Zinc in Neural Communication
It has been known that zinc is an essential trace
element needed for normal growth and development, and a recent study by
Salk
Institute investigators shows it to be an integral part of ion channels.
The study, which appears in the current issue of Nature
Structural Biology, may explain why zinc deficiency has been linked
to cognitive impairment. "We don't know yet what zinc is doing, but it
is definitely a component in these essential structures," said Senyon Choe,
an assistant professor at
The Salk Institute for Biological Studies and senior author on the
study. "And it was surprising--at first we tried to disregard it, thinking
it must be a contaminant, but, of course as you try to disprove it, it
keeps coming back."
Ion channels give rise to neural communication by
regulating sodium, chloride, potassium and calcium conductance across the
membrane. This ionic flow gives rise to various membrane voltages. Calcium
channel conductance is associated with transmitter release and abnormalities
in potassium channels, which give rise the resting potentials and action
potentials, have been found in some epileptics and in persons with both
insulin-resistance and mobility disorders.
In the Salk study, Choe and his colleagues used
X-ray crystallography to resolve the structures of four potassium channels
from the sea slug Aplysia. The channels, called Shaw, Shab, Shal
and Shaker, represent the four classes of potassium channels found in all
higher organisms, including humans. With the exception of Shaker, all of
the channels contained four zinc atoms in analogous positions.
"Each channel resembles a funnel," said Choe, "and
the zinc elements ring the end that empties into the cell's interior."
Neuroscientists have known for decades that dyes
that bind to zinc stain brain cells in unique patterns, indicating that
zinc should have a role in brain function. Moreover, many animal
studies have demonstrated that zinc deficiency causes impairments in learning,
and studies have shown that zinc can enhance learning in undernourished
children. The nature of zinc's organization in the brain, however, had
been unclear.
"Now we know that zinc is embedded within structures
that are absolutely critical for nerve cell activity," said Choe. "Furthermore,
the amino acids that cradle the zinc atoms are completely conserved among
the three classes of channels, telling us that during evolution there has
been selective pressure to keep that zinc in place."
All four kinds of Aplysia potassium channels studied
by Choe and colleagues have analogs in the human nervous system, so the
investigators believe that their studies of zinc's role in Aplysia
channel function are directly relevant to understanding its function in
the human brain.
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Gene's Role in Parkinson's Disease may be Minimal
Genetic factors do not appear to play a significant
role in causing the most common form of Parkinson's disease (PD), according
to a study to be published in the January 27, 1999 issue of the Journal
of the American Medical Association (JAMA). This epidemiological
study, the largest of its kind to investigate the role of genetic or environmental
causes of PD, examined 19,842 white male twins enrolled in a large registry
of World War II veteran twins.
"This study cuts a wide swath of research opportunities
into causes of Parkinson's disease by suggesting that heredity is not a
major etiologic component in the largest group of PD patients, those whose
disease began after age 50," said Michael D. Walker, M.D., Director of
the Division of Stroke, Trauma, and Neurodegenerative Disorders at the
National Institute of Neurological Disorders and Stroke (NINDS). The study
was funded by the NINDS and The Valley Foundation of Los Gatos, California,
a non-profit organization that supports a variety of health care causes,
including PD.
For many years, researchers have speculated about
the causes of PD, with the primary considerations being genetic determinants
and environmental factors. The current study suggests that typical PD --
defined as PD diagnosed after age 50 -- has no genetic component, while
the opposite was observed in a small subset (six pairs) of identical and
fraternal twins whose PD was diagnosed before age 51 in at least one twin.
Investigators concluded that undetermined environmental factors, not genetics,
are likely triggers of typical PD and they suggest that research concerning
a genetic link to PD be directed toward subjects with earlier onset of
the disease.
Twin studies have proven particularly useful in
distinguishing the relative contributions of genetics and environment to
the cause of various diseases. In the JAMA study, the investigators theorized
that if PD had a genetic basis, both individuals in an identical twin pair
would be expected to develop the disease (since they have the exact same
genetic make-up). Instead, they found that PD most commonly occurred in
only one member of a twin pair, whether the pair was identical or fraternal.
"Since purely genetic Parkinson's disease appears
to be rare, investigations of genetic forms of parkinsonism, such as in
families with multiple-affected generations, will help us to identify the
underlying disease mechanisms," said principal investigator Caroline M.
Tanner, M.D., Ph.D., of The Parkinson's Institute in Sunnyvale, California,
and lead author of the JAMA study.
Study subjects were part of the National Academy
of Sciences/National Research Council World War II Veteran Twins Registry,
which consisted of 15,924 pairs of white male twins when established in
1959. This study attempted to contact all 19,842 individual twins believed
to be alive as of 1992. Pairs were excluded if both twins could not be
located, refused to participate, or were known to be dead. If one twin
was eligible and the other refused to participate, had dementia, or was
dead, a proxy informant was used, either the participating twin brother,
a previously provided contact, or a commercially available database.
In brief interviews, all study subjects received
screening for suspected Parkinsonism, dementia, cerebrovascular disease,
eye disease, cancer, and possible risk factors for these diseases. This
cohort was ideal for the study, as they had reached an age range of increasing
risk for PD. Twins diagnosed in the study as having possible or probable
PD were found to exhibit at least two of the four standard symptoms of
parkinsonism ¾ tremor, rigidity, postural instability, and bradykinesia
(gradual loss of spontaneous movement).
More than half a million Americans have PD, a chronic
and progressive motor system disorder that strikes men and women almost
equally. The disease usually affects people over age 50, with the average
age of onset at 60 years. Up to 50,000 new cases are diagnosed each year.
Currently the disease has no cure; standard treatment usually involves
the drug levodopa, or L-dopa, but symptoms may return following long-term
use of this drug.
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What Type of Neural Activity Promotes Development of Connections?
The "use-disuse"
hypothesis of neural development has long been accepted as the method by
which synaptic connections in the brain become established. For instance;
It has been tacitly assumed that activity in a particular synapse will
promote strengthening of a connection, whereas inactivity in a particular
synapse would cause either translocation (movement) or elimination of the
synapse. Results of a recent study appearing in the Jan. 28, 1999
issue of Nature complicates
this simplistic view of synaptic development, and suggest that "inappropriate"
synaptic activity may be more influential in eliminating synapses, as compared
to no synaptic activity at all. The study shows that the loss of connections
between neurons in the brain is not entirely the result of inactivity,
as was previously thought, but a consequence of neural activity that is
"inappropriate" for the given neural system.
It has been known
that experiences during early postnatal life determine how connections
are estabilished between neurons in the brain. Many more neurons and syanpses
are made during fetal life than will be used postnatally, and some of these
connections are retained and made stronger, while others are weakened and
eventually lost. This refinement of synapses is responsible for the acquisition
of brain function through life. While the mechanisms of experience-dependent
brain modification normally are responsible for the improvement of
function during development, in some clinical conditions they can actually
lead to a loss of function. For example, a loss of function during infant
development can result when one eye is deprived of normal visual experience,
as can occur with a cataract. As a consequence of this deprivation, connections
within visual centers of the brain are weakened to the point that "blindness"
occurs. The "blindness" actually occurs as a result of a changes in central
neural connections, so that blindness persists even when normal visual
functions are returned to the eye by removal of the cataract.
Visual deprivation
experiments have been used to study the effects of sensory deprivation
on development of central neural connections. And, in these experiments
unilateral occlusion of the eye will cause alterations in central visual
connections receiving input from the occluded eye. However, receptors
of the eye remain active even with the eyelids closed, and the main difference
between occlusion and "non-occlusion" is the pattern
of activity that is conveyed in the optic nerve.. The activity generated
by a seeing eye is like the signals of a well-tuned radio station, and
the activity generated by an occluded eye is more like static. In consideration
of these facts, researchers at the Howard Hughes Medical Institute and
Department
of Neuroscience at Brown University tested the validity of a theory
developed by Nobel Laureate Leon Cooper and associates at Brown University.
The theory suggests that "static" in the deprived eye actually causes connections
to become weaker or eliminated.
Graduate student
Cindi Rittenhouse and professors Harel Shouval, Michael Paradiso and Mark
Bear tested that theory in animals. Half of the animals received a drug
that blocked all electrical activity in one eye; the other half simply
had their eyelids closed. In contrast to the conventional view, the researchers
found that neural connections associated with the occluded eye were altered
to a greater extent than connections in which all activity was eliminated.
"This result
is counterintuitive. You would expect that complete absence of activity
would be most severe," said Bear. "It is important to understand the mechanism
by which connections are weakened -- Not only because such understanding
may yield insight into ways that at least one type of blindness can be
avoided, but also because this is a fundamental part of normal brain development."
These findings
seem to support that notion that there is some "optimal" level of neural
activity that is needed in developing brain circuits, but it is currently
unclear how developing systems gauge what is "appropriate" activity and
what is not. Moreover, the levels of "appropriate" activity probably
differs in various systems.
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Life
Among Sick Brain Cells
For years, it
has been believed that brain cells do not regenerate following brain damage.
But a new study found that some brain cells are actually stimulated to
regenerate following damage, a discovery that opens the door to treating
brain injury. According to the authors, they have provided the first evidence
that a certain type of brain cell -- called a stem cell -- demonstrates
the ability to regenerate after brain damage.
The research
was performed by inducing stroke in rodents. Following the blockage of
blood flow and decreased oxygen and glucose delivery to the brain -- a
condition known as ischemia -- researchers found a 12-fold increase in
the birth of new cells in the dentate gyrus of the hippocampus, a region
of the temporal lobe that is crucial in laying down all long term memories.
Following the ischemia, half of the newborn cells became neurons and a
quarter of the cells became glial cells.
"(Previous) data
show that new neurons are born in the brains of adult monkeys and in the
brains of adult humans," said Frank Sharp, M.D., of the Department
of Neurology, University of California-San Francisco and one of the
study's investigators. "It is not known whether there are new neurons born
in the brains of humans following stroke. We certainly think they would
be."
Sharp said the
research is the first to demonstrate that neural stem cells divide into
neurons and astrocytes following ischemia. Though neurons are the information
cells in the brain, gilal cells called astrocytes have important functions
for maintaining the metabolic health of the neurons (Module
5: Principles of Psychobiology). Gilal cells have long
been considered as only supporting cells, but recent research in the past
few years has suggested that these cells are just as important in the transfer
of information from the brain to other parts of
the body.
The birth of
new neurons and glial cells following a stroke could provide a new way
to treat stroke survivors, according to Sharp. Recent studies have shown
that new neurons are born in the human brain as well, and the hope for
the future is that these cells to be stimulated to improve function even
more.
"Our studies
show that the newborn neurons do not occur because of the death of neurons
in ischemic brain," says Sharp. "We are able to produce a degree of ischemia
that stimulates neuronal birth without killing other neurons. Therefore,
ischemia itself stimulates the new neurons. We believe that this represents
a protective response that facilitates memory function that may be disturbed
even with brief ischemia."
More
on transplantation after stroke from National Public Radio...
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Nature-Nuture
in Stem Cell DNA
Research pertaining to stem cells, and the possibility of using stem cells to promote neural repair, has received a large amount of attention within the last 6 months. Together with observing that brain stem cells may give rise to neuronal development in adults, it also seems possible that stem cells have some inherant ability to determine what type of cell to produce. Recent data are discussed in an NPR interview...
More
on stem cells from National Public Radio...
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Sensory Experience Alters The Development Of Both Sensory and Motor Areas of the Neocortex
Sensory experience plays a significant role in guiding development of the
nervous system. Data which substantiate this conclusion have been
obtained primarily from sensory deprivation experiments which have generally
shown that depriving animals of specific sensory stimuli alters normal
development of the corresponding sensory area of the brain. However,
it now seems that the effects of sensory deprivation may be more global,
insofaras sensory deprivation appears to not only influence development
of the specific sensory brain region, but also the development and
organization of areas involved in corresponding voluntary movement. A study
published in The Journal of
Neuroscience supports this conclusion. "The research suggests
that sensory feedback to the brain's motor cortex system is one of the
major driving forces that shapes motor function during development," says
the study's author, George Huntley of The
Mount Sinai School of Medicine in New York. "The discovery also (again
confirms) that early in development there is a restricted time period
where the motor system is most susceptible to modification and refinement
by incoming sensory signals."
In the study, Huntley tested the effects of somatosensory deprivation by
trimming the whiskers of rats. Rats use the whiskers on their
snouts like humans use their fingertips to explore and discriminate surface
features such as texture. The whisker region in the rat somatotopic
map is very large, similar to the digit and lip region in human.
In rat, each whisker is precisely mapped onto a relatively large region
of the somatosensory neocortex (Module
5: Principles of Psychobiology) called
a "whisker barrel", and in all animals with neocortex, the primary somatosensory
neocortex is connected directly to the adjacent primary motor cortex.
Whiskers are moved by motor areas of the brain, which cause the whiskers
to move back and forth during voluntary movement. This whisker-trimming
manipulation therefore made the animals experience abnormal sensory inputs
to both sensory and motor areas of the neocortex. Huntley
examined a group of adult rats that had the whiskers on one side of their
snout trimmed starting at birth and another group that had their whiskers
trimmed starting in adulthood.
During adulthood, a electrode implanted in the animals' motor cortex revealed
representations of motor activity (Module
5: Principles of Psychobiology).
The results showed significantly smaller representations of motor activity
and some abnormal motor activity patterns in the rats that were trimmed
at birth. The adult-trimmed group had no significant changes in the size
of their representations of motor activity maps, but they did show some
slight changes in the form of motor activity elicited.
These results reinforce the view that sensory experience during early development
modifies both the organization of the somatosensory neocortex and the primary
motor neocortex. It is currently unclear whether deprivation in other
sensory
modalities produce corresponding alterations in motor function. One
human implication could be that visual defects early in life may affect
not only the sensory brain areas that process vision, but also the motor
cortical areas that mediate visually-guided motor responses.
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Reorganization
of the Somatosensory Thalamocortical Relay
The early anatomists adopted the term thalamus
to mean the "center" or "home" of the brain, and this name was apparently
chosen on the basis of the physical location of the thalamus in relation
to the surrounding brain regions in human. Indeed, we now know that
the thalamus serves as the highest level of information processing in species
that lack the neocortex, and the major ascending sensory relay in species
that do possess neocortex (Module
5: Principles of Psychobiology). Although
it has been known for some time that the organization of connections within
the neocortex is both maintained and modified by sensory activity, it now
seems clear that the thalamus can also reorganize after sensory deprivation.
Researchers at Wake Forest University
School of Medicine and the University
of California at Davis reported these results in the Nov. 6, 1998 issue
of Science.
The newly published study follows a 1991 report
(Science) which confirmed
that the somatosensory cortex itself remodels after injury. Both reports
added to the mounting evidence that the brain is not fixed and unchanging
after infancy, as had been previously thought, but is able to establish
new connections. The term "plasticity" has been used to describe the fact
that the connections within brain can change. Tim P. Pons, Ph.D.,
professor of surgical sciences (neurosurgery) and professor of physiology/pharmacology
at Wake Forest and Edward C. Jones, Ph.D., director of the Center for Neuroscience
at the University of California-Davis, said that a portion of the thalamus
in nonhuman primates was completely reorganized after the nerves relaying
sensory information from the arms were severed in the periphery.
The actual work involved experiments stimulating
the face after impulses from the entire upper arm and hand were prevented
from reaching the brain for a period of time. It is well-established that
the somatosensory thalamus (VPL) (Module
5: Principles of Psychobiology) is organized somatotopically,
similar to the somatosensory neocortex, such that the most ventral and
medial area of VPL thalamus receives face information, and the more lateral
region receives arm and digit information. Following the nerve transection,
VPL thalamus had "rewired" so that regions which previously received sensory
arm and hand information (VPL thalamus) now responded to facial stimulation.
"When the face takes over the hand representation,
the brain still interprets the impulses as coming from the hand," Pons
said. The findings were strikingly similar to clinical case studies
of people who had undergone upper arm amputations. When those investigators
touched these amputees in certain parts of the face, the patients had sensations
that seemed to be coming from the missing limb. "This is a very plausible
explanation for phantom limb sensations and especially phantom
pain sensations," Pons said.
"We have identified the thalamus as being a critical
component for that plasticity that is exhibited at the somatosensory neocortex.
We're not sure that these changes don't also occur at the spinal level,"
Pons said, "but we doubt it is a factor because of the severe degenerative
changes seen anatomically in these animals." "This is exciting because
it could be the underpinning of the neurobiological basis for recovery
of function after stroke or damage to the nervous system." "We had shown
that at least one-third of the entire somatosensory cortex is capable of
reorganization, and this latest work shows that at least one-third of the
thalamus is also capable of a similar type of reorganization."
While he said it was premature to speculate about
direct applications of the research to people, the researchers will be
trying to harness the plasticity of the brain when it helps -- such as
after a stroke -- and halt the plasticity when it causes problems, such
as epilepsy, Parkinson's disease and Alzheimer's disease.
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